SEATTLE, May 1 -- A diet that's high in vegetables, nuts, and fish but low in fatty dairy products may help protect against Alzheimer's disease, researchers said here.

Patients in the highest tertiles of such a diet had a 42% reduced risk of developing Alzheimer's, Yian Gu, Ph.D., of Columbia University, and colleagues said at the American Academy of Neurology Meeting.

"There was a significant relationship for the seven nutrients that are most consistently associated with Alzheimer's disease," Dr. Gu said.

Dr. Gu and her colleagues used the Reduced-Rank Regression model to analyze dietary patterns that might explain the variation of nutrients that is believed to be related to disease risk.

They evaluated the diet via those seven Alzheimer's disease-related nutrients: saturated fats, monounsaturated fats, omega-3 fatty acids, omega-6 fatty acids, vitamin E, vitamin B12, and folate.

The researchers prospectively assessed 2,136 healthy elderly patients in New York who
provided dietary information. Participants were evaluated with the same standardized neurological and neuropsychological measures every one-and-a-half years.

A total of 251 patients developed Alzheimer's disease over the four-year follow-up period.
In a multivariate analysis, the researchers found that a diet high in omega-3, omega-6, folate, and vitamin E, and low in saturated fat and B12, was strongly associated with lower risk of Alzheimer's disease.

Compared with the lowest scores for dietary pattern, the middle and highest tertiles had significantly reduced risks of developing Alzheimer's (HR 0.77, 95% CI 0.56 to 1.05 and HR 0.58, 95% CI 0.40 to 0.84, respectively, P<0.01).

Dr. Gu said the B12 finding was "surprising" since deficiency of the nutrient is associated with dementia. However, a major dietary source of B12 is meat, which is also a large source of saturated fat, she said.

The protective diet was characterized by higher intakes of cruciferous vegetables, green-leafy vegetables, fish, nuts, and tomatoes, and by a lower intake of high-fat dairy products.

Dr. Gu said that further study of Alzheimer's disease-related nutrients can better identify dietary patterns that relate to disease risk. .......report in MedPage Today

DENVER, April 21 -- Reprogrammed immune cells could become targeted "killing machines" against prostate cancer, a researcher said here.

In the early stages of a phase I study, these reprogrammed T cells sharply reduced the levels of prostate specific antigen (PSA) in two patients with metastatic prostate cancer, according to Richard Junghans, M.D., Ph.D., of the Roger Williams Medical Center in Providence, R.I.

Within a few weeks of the infusion of the engineered cells, one patient's PSA level had fallen by half and the other's by 75%, Dr. Junghans reported at the annual meeting of the American Association for Cancer Research. T cells, Dr. Junghans told reporters, are the "perfect killing machines" when faced with a cell infected with a virus. "We have to fool the T cells into thinking that the cancer has a virus infection," he said.

To do that, he and colleagues isolate a patient's T cells from a blood sample and use genetic engineering techniques to make them sensitive to a molecule that only occurs in prostate cancer -- prostate specific membrane antigen, or PSMA.

Over a period of weeks, the modified cells are amplified in culture. Meanwhile the patient undergoes chemotherapy to knock down his remaining lymphocytes, creating "hematopoietic space" for the engineered T cells.

Finally, he said, the cells are infused into the patient and begin attacking cells that express PSMA. A marker for that activity, Dr. Junghans said, is the level of prostate specific antigen.
The falling levels of PSA in the two patients treated so far were obtained despite the low dose of cells they were given -- about a billion each.

The researchers plan to test that dose in one more patient and then escalate the dose -- first to 10 billion in six patients and then to 100 billion in another six.

In the two patients treated so far, the falling PSA levels appeared to have bottomed without reaching zero -- possibly because the methods used to activate them caused them to enter a resting state without completely eradicating the cancer cells, Dr. Junghans said.

With the higher doses, he said, he hopes to see PSA levels fall all the way to zero.
"We are very hopeful that when we get to higher doses," he said, "all those activated (cells) may get us to 100% suppression before they go to the resting state."

Dr. Junghans said the redirected T cells are a "brave new world" for cancer treatment. "I predict the FDA will have approved one of these designer T-cell constructs -- if not this one, then another one -- as standard therapy in the next five or so years," he said.

Dr. Junghans' approach is a new twist on ideas that have been around for "two decades or more," said Louis Weiner, M.D., of Washington's Lombardi Cancer Center, who was not part of the research.

"What Dr. Junghans and colleagues have done is to really combine two critical elements" -- redirecting the T cells and creating space for them by chemotherapy, Dr. Weiner said.

He said while the idea is intriguing and the early results promising, "at the end of the day, we will need properly conducted efficacy trials."

But "the early returns are sufficiently encouraging that I certainly hope they continue doing the work," he said.
MedPage Today

SEATTLE, Feb. 18 -- Middle-age and older adults who prefer a mental workout to passive activities, such as watching TV, may be less likely to develop memory loss as they age, researchers said.

Mentally stimulating social activity and reading in middle age reduced the likelihood of mild cognitive impairment in old age by more than 40%, found Yonas E. Geda, M.D., of the Mayo Clinic in Rochester, Minn., and colleagues.

After age 65, reading, making crafts, using the computer, playing games, and watching less TV were associated with 30% to 50% lower risk of mild cognitive impairment, Dr. Geda's group reported in a case-control study to be presented at the American Academy of Neurology meeting here.

Dr. Geda said these findings provide concrete evidence for the "use it or lose it" axiom. "This means perhaps aging does not have to be a simple passive process."

In the multivariate analysis adjusted for age, sex, and education, the researchers found the following activities done over the prior year late in life protective against mild cognitive impairment:

• Reading books (odds ratio 0.67, 95% confidence interval 0.49 to 0.94)
• Playing games (OR 0.65, 95% CI 0.47 to 0.90)
• Crafting activities, such as quilting or pottery (OR 0.66, 95% CI 0.47 to 0.93)
• Computer activities (OR 0.50, 95% CI 0.36 to 0.71)
• Watching television less (OR 0.48 for fewer than seven hours per day versus more, 95% CI 0.27 to 0.86)

Dr. Geda cautioned that the findings were based on patients' memories of activities and need to be confirmed in prospective studies.

full story and video in MedPage Today

IOWA CITY, Iowa, Feb. 11 -- The difficult judgment call on whether Alzheimer's patients are safe to drive can be helped by a battery of cognitive tests, researchers here said.

"By measuring driver performance through off-road tests of memory, visual, and motor abilities, we may be able to develop a standardized assessment of a person's fitness to drive," Dr. Dawson said.

To determine whether performance on tests of cognition, visual perception, and motor function could predict the level of safety in licensed drivers with early Alzheimer's, the researchers conducted a controlled trial of 40 patients with mild disease and 115 patients without dementia.

"Given that driving puts demands on diverse cognitive functions, it is unlikely that a test of any single cognitive ability will be an accurate predictor of driving safety," the researchers said.

The study may have been limited by a lack of investigation of other environmental factors, such as having family members in the vehicle and time of day, as well as a possible lack of generalizability because only seven of the 40 patients in the experimental group were women.

Still, the researchers concluded that for predicting safety errors within the Alzheimer's disease group, "off-road neuropsychological tests of cognition, vision, and motor abilities gave additional information above and beyond diagnosis alone. Hence, performance on these tests can be helpful when predicting whether a patient with Alzheimer's disease can safely drive a vehicle."
full story in Medpage Today

Kapil D. Sethi, MD, Professor of Neurology; Director, Movement Disorders Program, Medical College of Georgia, Augusta
Medscape Today

STANFORD, Calif. — You come into a doctor’s office with severe knee pain. The physician orders an MRI, which reveals substantial loss of cartilage — osteoarthritis, that is—in your knee joint. At this point, not much can be done beyond gulping down palliatives and trying to keep your weight off the joint. But the damage may have started building as much as 20 years earlier, possibly due to a traumatic injury to the affected joint.

Just ask Garry Gold, MD, an associate professor of radiology at the Stanford University School of Medicine. Now 45, Gold sustained a knee injury 20 years ago while playing in a pickup basketball game. These days, he’s starting to wish his house, currently being remodeled, didn’t have any stairs.

Gold, who has been diagnosed with osteoarthritis, is working with an imaging technology called sodium MRI to diagnose osteoarthritis as long as decades before the onset of physical symptoms. That may spawn new therapies that could possibly have blocked his disease before it put an end to his basketball days.

Using the new imaging technology, Gold and colleagues have been able to spot, soon after such an injury, telltale signs of cartilage deterioration consistent with the development of osteoarthritis.

Sodium MRI has been around for years, but until recently it couldn’t be used in clinical settings. For one thing, the magnets employed to excite sodium atoms were too puny, making crisp resolution possible only with tiny creatures such as mice. Gold and his colleague Brian Hargreaves, PhD, assistant professor of radiology, have designed improved magnets and software to scale up the technology for human application.

Gold and Hargreaves’ project is being conducted with funding from the National Institutes of Health and GlaxoSmithKline, an international pharmaceutical company. Neither researcher owns stock in, or receives consulting fees from, the company.

Catching osteoarthritis during its stealth phase may spur clinical trials that would be prohibitively time-consuming and costly if standard MRI were employed, because of the huge lag from the time of an ACL injury until the time cartilage deterioration can be detected by that old method.

With sodium MRI, cohorts of treated vs. untreated at-risk patients could be imaged over time to see if, within a few years of the injury, a drug or a lifestyle change is reducing or arresting the loss of glycosaminoglycan from the ligament. Once promising drugs or lifestyle changes are identified, they could then be administered to at-risk patients long before symptoms surface, Gold said.

As for Gold himself, he has yet to see what his own damaged knee looks like under sodium MRI. The 6-foot-6 once-avid amateur basketball center’s knee is too big for even his improved new experimental apparatus to fit. It’s probably too late for any kind of imaging to do Gold much good now, anyway. He already knows he’s got arthritis. “I don’t even want to look,” he said.

Full story & Video: Stanford School of Medicine

The original Dear Abby, now living with Alzheimer's disease, once positively impacted millions of lives. Her daughter, the current Dear Abby, shares what her life is like now.

http://www.empowher.com/community/herstory/video-herstory-dear-abby-shares-what-her-alzheimers-mothers-life-today

High neuroticism has been associated with a greater risk of dementia, and an active/socially integrated lifestyle with a lower risk of dementia. The aim of the current study was to explore the separate and combined effects of neuroticism and extraversion on the risk of dementia, and to examine whether lifestyle factors may modify this association.
NEUROLOGY 2009;72:253-259

STANFORD, Calif. — Scientists at the Stanford University School of Medicine and at UC-San Francisco have succeeded in isolating stem cells from human testes. The cells bear a striking resemblance to embryonic stem cells — they can differentiate into each of the three main types of tissues of the body — but the researchers caution against viewing them as one and the same....full story in Stanford School of Medicine Medical News

January 8, 2009 — Results of a randomized trial show that compared with best medical therapy, deep brain stimulation (DBS) increased "on" time without dyskinesias and improved motor function as well as quality of life at 6 months in patients with moderate to severe Parkinson's disease (PD), but at the cost of increased serious adverse events (SAEs)........full story
Medscape Today

LONDON, Jan. 8 -- For patients with Alzheimer's disease, antipsychotic medications substantially increase one-year mortality risk, researchers found. Patients who continued on their antipsychotic regimen were 42% more likely to die over a one-year... full story

MedPage Today

Don't let osteoporosis rob your bones of their strength. Here are some exercises to prevent or treat this common bone disease.
The Mayo Clinic

Osteoporosis treatment may involve medication along with lifestyle change. A Mayo Clinic specialist answers some of the most common questions about osteoporosis treatment.
The Mayo Clinic

Technologies like a flu-tracking app and phone wipes could help you get through flu season unscathed.
PC Magazine

NEW YORK (Reuters Health) Dec 29 - Tests show that certain MRI machines may demagnetize magnets used in cochlear implants to couple external and implanted components, according to a report in the December issue of Otolaryngology--Head and Neck Surgery.
Medscape Today

December 30, 2008 — Memory decline with age appears partly explained by increased blood glucose levels that cause decreased activity in the dentate gyrus, a new study published in the December issue of the Annals of Neurology suggests.

Since blood glucose levels tend to rise with age, this study suggests that improving blood glucose regulation may be a good way to ameliorate age-related memory decline, said Dr. Small.

"Whether through physical exercise, diet, or drugs, this research suggests that improving glucose metabolism could help some people avert the cognitive slide that occurs in many of us as we age," he said.

Their study suggests that moderating blood glucose levels, through physical exercise, diet, or medication, may aid in preventing cognitive decline, he added.

Nevertheless, "the results showed a clear difference in cognitive performance as a function of diet . . . [and] the data suggest that diet can affect more than just weight," Dr. Taylor said in a statement. "The brain needs glucose for energy, and diets low in carbohydrates can be detrimental to learning, memory and thinking."
Medscape Today

Judicious Drinking Associated with Reduced Risk of Dementia
MAYWOOD, Ill., Dec. 30 -- Having a drink only occasionally may reduce the risk of dementia, perhaps because long exposure to low alcohol levels help brain cells survive other stresses, researchers here said.
Medscape Today - Full story

NEW YORK, Dec. 30 -- Lowering blood glucose levels may help lessen the cognitive decline of normal aging, even in diabetes-free patients, researchers here said.
Medscape Today - Full story

The U.S. Food and Drug Administration today announced it will require the manufacturers of antiepileptic drugs to add to these products' prescribing information, or labeling, a warning that their use increases risk of suicidal thoughts and behaviors (suicidality). The action includes all antiepileptic drugs including those used to treat psychiatric disorders, migraine headaches and other conditions, as well as epilepsy.

The FDA is also requiring the manufacturers to submit for each of these products a Risk Evaluation and Mitigation Strategy, including a Medication Guide for patients. Medication Guides are manufacturer-developed handouts that are given to patients, their families and caregivers when a medicine is dispensed. The guides will contain FDA-approved information about the risks of suicidal thoughts and behaviors associated with the class of antiepileptic medications.

"Patients being treated with antiepileptic drugs for any indication should be monitored for the emergence or worsening of depression, suicidal thoughts or behavior, or any unusual changes in mood or behavior,” said Russell Katz, M.D., director of the Division of Neurology Products in the FDA's Center for Drug Evaluation and Research. “ Patients who are currently taking an antiepileptic medicine should not make any treatment changes without talking to their health care professional.”

The FDA today also disseminated information to the public about the risks associated with antiepileptic medications by issuing a public health advisory and an information alert to health care professionals. Health care professionals should notify patients, their families, and caregivers of the potential for an increase in the risk of suicidal thoughts or behaviors so that patients may be closely observed.

The FDA's actions are based on the agency's review of 199 clinical trials of 11 antiepileptic drugs which showed that patients receiving antiepileptic drugs had almost twice the risk of suicidal behavior or thoughts (0.43 percent) compared to patients receiving a placebo (0.24 percent). This difference was about one additional case of suicidal thoughts or behaviors for every 500 patients treated with antiepileptic drugs instead of placebo.

Four of the patients who were randomized to receive one of the antiepileptic drugs committed suicide, whereas none of the patients in the placebo group did. Results were insufficient for any conclusion to be drawn about the drugs' effects on completed suicides. The biological reasons for the increase in the risk for suicidal thoughts and behavior observed in patients being treated with antiepileptic drugs are unknown.

The FDA alerted health care professionals in January 2008 that clinical trials of drugs to treat epilepsy showed increased risk of suicidal thoughts and actions. In July 2008, the FDA held a public meeting to discuss the data with a committee of independent advisors. At that meeting the committee agreed with the FDA's findings that there is an increased risk of suicidality with the analyzed antiepileptic drugs, and that appropriate warnings should extend to the whole class of medications. The panel also considered whether the drugs should be labeled with a boxed warning, the FDA's strongest warning. The advisers recommended against a boxed warning and instead recommended that a warning of a different type be added to the labeling and that a Medication Guide be developed.

Acting under the authorities of the Food and Drug Administration Amendments Act of 2007 (FDAAA), the FDA is requiring manufacturers of antiepileptic drugs to submit to the agency new labeling within 30 days, or provide a reason why they do not believe such labeling changes are necessary. In cases of non-compliance, FDAAA provides strict timelines for resolving the issue and allows the agency to initiate an enforcement action if necessary.

The following antiepileptic drugs are required to add warnings about the risk of suicidality:
Carbamazepine (marketed as Carbatrol, Equetro, Tegretol, Tegretol XR)
Clonazepam (marketed as Klonopin)
Clorazepate (marketed as Tranxene)
Divalproex sodium (marketed as Depakote, Depakote ER)
Ethosuximide (marketed as Zarontin)
Ethotoin (marketed as Peganone)
Felbamate (marketed as Felbatol)
Gabapentin (marketed as Neurontin)
Lamotrigine (marketed as Lamictal)
Lacosamide (marketed as Vimpat)
Levetiracetam (marketed as Keppra)
Mephenytoin (marketed as Mesantoin)
Methosuximide (marketed as Celontin)
Oxcarbazepine (marketed as Trileptal)
Phenytoin (marketed as Dilantin)
Pregabalin (marketed as Lyrica)
Primidone (marketed as Mysoline)
Rufinamide (marketed as Banzel)
Tiagabine (marketed as Gabitril)
Topiramate (marketed as Topamax)
Trimethadione (marketed as Tridione)
Valproic Acid (marketed as Depakene, Stavzor Extended Release Tablets)
Zonisamide (marketed as Zonegran)

Some of these medications are also available as generics.

Health care professionals and consumers may report serious adverse events or product quality problems with the use of this product to the FDA's MedWatch Adverse Event Reporting program either online, by regular mail, fax or phone.

-- Online : http://www.fda.gov/MedWatch/report.htm

-- Regular Mail : use postage-paid FDA form 3500 available at: http://www.fda.gov/bbs/topics/NEWS/2008/www.fda.gov/MedWatch/getforms.htmand mail to MedWatch, 5600 Fishers Lane , Rockville , MD 20852-9787

-- Fax: (800) FDA-0178

-- Phone: (800) FDA-1088

For more information
Information for Health Care Professionals and Public Health Advisory: http://www.fda.gov/cder/drug/infopage/antiepileptics/default.htm

U.S. Food and Drug Administration - FDA News

UMEA, Sweden, Dec. 16 -- Long-term mortality in locally advanced prostate cancer was improved by 50% when external-beam radiation was added to hormone therapy, found researchers here.

At 10 years, prostate specific mortality was 23.9% for those given only hormone therapy versus 11.9% for the combination therapy arm, wrote Anders Widmark, M.D., of Umea University, and colleagues in the Scandinavian Prostate Cancer Group.

The findings derived from evaluable results from 875 men, 439 who received three months of total androgen blockage followed by continuous hormone therapy using flutamide, and 436 who had the same hormone regimen combined with external beam radiation.

Yet Drs. Tan and Parker concluded that the findings represented a pivotal trial that should "change current practice, making long-term hormonal therapy plus radical radiotherapy the standard of care for men with locally advanced prostate cancer."

MedPage Today

URBANA, Ill., Dec. 11 -- Older individuals may be able to stem the age-related decline in cognitive function by playing video games, researchers here found.

Nearly two dozen hours of playing a strategic video game over several weeks led to increased performance on four out of six tests of executive function, Arthur Kramer, Ph.D., of the University of Illinois at Urbana-Champaign, and colleagues reported in the December issue of Psychology and Aging.

"Whether similar transfer effects would be observed with video-game-based training to everyday cognition in older adults is a both theoretically as well as practically important question, especially given the rapid expansion of commercial products and computer programs touted to improve the cognitive abilities of older adults," the researchers said.

Previous studies have shown that training individuals in a particular cognitive task can enhance performance on that specific task, the researchers said.

But opinions are mixed on whether training can result in improvements in an array of cognitive skills, they said.

Commercially available computer products that claim to improve cognitive function, he said, tend to "take a more piecemeal approach."

The authors acknowledged that the study was limited by the fact that the control group did not play a video game.

Future studies should evaluate whether the improvements in laboratory-based measurements of cognitive function translate into everyday activities like driving a car or working in a busy office, they said.

MedPage Today

LA JOLLA, Calif., Dec. 4 -- Alzheimer's patients with coexisting obstructive sleep apnea may derive cognitive benefits from treatment with continuous positive airway pressure (CPAP), investigators here concluded.

CPAP led to significant improvement on a neuropsychological test battery compared to baseline, Sonia Ancoli-Israel, Ph.D., of the University of California San Diego, and colleagues reported in the November issue of the Journal of the American Geriatrics Society.

"Although it is unlikely that obstructive sleep apnea causes dementia, the lowered oxygen levels and sleep fragmentation associated with obstructive sleep apnea might worsen cognitive function," said Dr. Ancoli-Israel. "This study, which showed significant improvement in patients' neurological test scores after treatment with CPAP, suggests that clinicians who treat patients with Alzheimer's disease and sleep apnea should consider implementing CPAP treatment."

Alzheimer's patients have a high prevalence of obstructive sleep apnea. Estimates range from 70% to 80% of patients having at least five episodes of apnea or hypopnea per hour to 40% to 50% having 20 or more episodes per hour.

Some evidence has suggested that more severe dementia is associated with more severe obstructive sleep apnea, they continued.

Studies of CPAP treatment for sleep apnea in patients without dementia have demonstrated improvement in neuropsychological function. Whether CPAP would lead to similar improvement in patients with Alzheimer's disease had not been examined in a randomized, placebo-controlled trial.

After the first three weeks, the two groups did not differ in changes in neuropsychological scores. However, in a paired analysis at six weeks (at which time one group had received six weeks of therapeutic CPAP and the other three weeks), both groups had significant improvement that averaged 0.077 points (P=0.01).

The study was limited by the small sample size, which did not allow for analysis of specific cognitive tests, and by the short duration of the study.

"[Obstructive sleep apnea] may aggravate cognitive dysfunction in dementia and thus may be a reversible cause of cognitive loss in patients with Alzheimer's Disease," the authors concluded. "OSA treatment seems to improve cognitive functioning."

Co-author Jody Corey-Bloom, M.D., Ph.D., also of UC San Diego, commented that "any intervention that improves cognition in patients with Alzheimer's disease is likely to result in greater independence and less burden on their caretakers."

A previous report from the same study showed that CPAP significantly reduced daytime sleepiness, a common complaint of Alzheimer's patients, Dr. Corey-Bloom added.

MedPage Today

Starting on Jan. 1, New York City ambulances will take many cardiac arrest patients only to hospitals that use a delicate cooling therapy believed to reduce the chances of brain damage and increase the chances of survival, even if it means bypassing closer emergency rooms.

The move by the city’s Fire Department and Emergency Medical Service, after a year of preparation, indicates a shift away from the prevailing view among emergency workers and the public that how fast critically ill patients reach the hospital is more important than which hospital treats them.

It amounts to an endorsement by the Bloomberg administration of a labor-intensive, often expensive and still-developing therapy that smaller community hospitals say they lack the staffing and financial wherewithal to provide.

Some hospital officials fear that the policy could be unfair to these smaller hospitals, depriving them of income from emergency-room patients and hurting their reputations with the public.

Since the Fire Department sent letters to hospital chief executives this week informing them of the impending change, about 20 of the 59 hospitals with emergency rooms have said they will have cooling operations ready by the Jan. 1 deadline.

Dr. David J. Prezant, chief medical officer of the New York Fire Department, acknowledged the culture change and the possibility that some hospitals would feel slighted. But he argued that scientific data shows the survival rate of cardiac arrest patients treated with therapeutic hypothermia, as the cooling process is called, is so much better than with conventional treatment that it would be irresponsible not to provide it.

“Theoretically every closest 911-receiving hospital will be able to provide this service,” he noted. “Whether that will be a reality or not is not for me to say.”

New York joins a handful of other American cities, including Seattle, Boston and Miami, as well as Vienna and London, in requiring transport to hospitals with cooling systems. But given New York’s large population and concentration of hospitals, the policy may provide the largest test to date of therapeutic hypothermia.

Most patients who suffer total cardiac arrest outside hospitals die because their brains have been starved of oxygen. But studies show that if the pulse of patients can be restarted and the body temperature cooled to about 8 degrees Fahrenheit below normal, brain damage can be reduced or minimized.

Only those cardiac arrest patients revived enough to show a pulse and whose heart problems are not associated with some other trauma are eligible for the cooling treatment, Dr. Prezant said. In New York City, that represents 1,500 to 2,000 of the about 7,500 out-of-hospital cardiac arrest cases reported each year.

Dr. Prezant said that in deference to hospital finances, the city has set no requirements for the kind of cooling techniques hospitals must use — some may start with inexpensive saline solutions and plastic bags filled with ice, while others employ sophisticated equipment manufactured and aggressively promoted by companies like Alsius, Innercool Therapies and Medivance.

The American Heart Association endorsed cooling for some types of cardiac arrest patients after two studies on its effectiveness were published in The New England Journal of Medicine in 2002. One study found that 55 percent of the patients who received the cooling treatment ended up with moderate or no brain damage, compared with 39 percent who received standard treatment. About 41 percent of the cooled patients died within six months, compared with 55 percent of the others.

But hospitals have been slow to adopt the treatment because it requires a precision of temperature regulation that is difficult to achieve, constant vigilance and cooperation among nursing, emergency, cardiac and neurological units.

The research has shown that cooling is effective for cardiac arrest from ventricular fibrillation, in which the heart muscle wriggles ineffectively.

If a pulse can be restarted quickly enough — within a matter of minutes — with a defibrillator, such patients can walk away relatively unscathed. But if not, they become comatose and suffer a cascading series of cellular-level injuries to the brain, which frequently lead to permanent brain damage or death.

Inducing moderate cooling of the body within 6 hours, for 24 hours, followed by gradual warming, slows cerebral metabolism and seems to reduce such injuries, studies have shown. (The technique’s effectiveness on other medical problems, including traumatic brain injury, is more controversial.)

“It was a very slow process in terms of really getting it to take hold,” Dr. Mayer said of the cooling treatment. “One reason is that cardiac arrest patients have just been surrounded by this shroud of therapeutic nihilism. They come in after cardiac arrest, they’re intubated, in a coma, everybody’s reflex thought process in terms of caregivers is ‘Oh God, there’s nothing you can do for these people.’ ”

He said that his main motivation was not financial but experiential, and that he had been converted by seeing patients who were comatose and given up for dead recover full or near-full function after hypothermia.

The New York Times

Although aging puts people at greater risk for serious eye disease and other eye problems, loss of sight need not go hand in hand with growing older. Practical, preventive measures can help protect against devastating impairment. An estimated 40% to 50% of all blindness can be avoided or treated, mainly through regular visits to a vision specialist. Regular eye exams are the cornerstone of visual health as people age. Individuals who have a family history of eye disease or other risk factors should have more frequent exams. Don’t wait until your vision deteriorates to have an eye exam. One eye can often compensate for the other while an eye condition progresses. Frequently, only an exam can detect eye disease in its earliest stages. You can take other steps on your own. First, if you smoke, stop. Smoking increases the risk of several eye disorders, including age-related macular degeneration. Next, take a look at your diet. Maintaining a nutritious diet, with lots of fruits and vegetables and minimal saturated fats and hydrogenated oils, promotes sound health and may boost your resistance to eye disease. Wearing sunglasses and hats is important for people of any age. Taking the time to learn about the aging eye and recognizing risks and symptoms can alert you to the warning signs of vision problems. Although eyestrain, spending many hours in front of a television or computer screen, or working in poor light do not cause harmful medical conditions, they can tire the eyes and, ultimately, their owner (see below). The eyes are priceless and deserve to be treated with care and respect — and that is as true for the adult of 80 as it is for the teenager of 18. 5 common eye myths dispelled Myth: Doing eye exercises will delay the need for glasses. Fact: Eye exercises will not improve or preserve vision or reduce the need for glasses. Your vision depends on many factors, including the shape of your eye and the health of the eye tissues, none of which can be significantly altered with eye exercises. Myth: Reading in dim light will worsen your vision. Fact: Although dim lighting will not adversely affect your eyesight, it will tire your eyes out more quickly. The best way to position a reading light is to have it shine directly onto the page, not over your shoulder. A desk lamp with an opaque shade pointing directly at the reading material is the best possible arrangement. A light that shines over your shoulder will cause a glare, making it more difficult to see the reading material. Myth: Eating carrots is good for the eyes. Fact: There is some truth in this one. Carrots, which contain vitamin A, are one of several vegetables that are good for the eyes. But fresh fruits and dark green leafy vegetables, which contain more antioxidant vitamins such as C and E, are even better. Antioxidant vitamins may help protect the eyes against cataract and age-related macular degeneration. But eating any vegetables or supplements containing these vitamins or substances will not prevent or correct basic vision problems such as nearsightedness or farsightedness. Myth: It’s best not to wear glasses all the time. Taking a break from glasses or contact lenses allows your eyes to rest. Fact: If you need glasses for distance or reading, use them. Attempting to read without reading glasses will simply strain your eyes and tire them out. Using your glasses won’t worsen your vision or lead to any eye disease. Myth: Staring at a computer screen all day is bad for the eyes. Fact: Although using a computer will not harm your eyes, staring at a computer screen all day will contribute to eyestrain or tired eyes. Adjust lighting so that it does not create a glare or harsh reflection on the screen. Also, when you’re working on a computer or doing other close work such as reading or needlepoint, it’s a good idea to rest your eyes briefly every hour or so to lessen eye fatigue. Finally, people who stare at a computer screen for long periods tend not to blink as often as usual, which can cause the eyes to feel dry and uncomfortable. Make a conscious effort to blink regularly so that the eyes stay well lubricated and do not dry out.

FEATURED CONTENT: How the eye works The eye examination Cataract Glaucoma Age-related macular degeneration (AMD) Diabetic retinopathy Other common eye diseases of later life Presbyopia: Ready for reading glasses? Safeguarding your sight Reprinted from The Aging Eye: Preventing and treating eye disease – A Special Health Report from Harvard Medical School, © 2008 by Harvard University. All rights reserved. Harvard Health Publications Harvard Medical School

CHICAGO, Dec. 1 -- Older adults who exercise regularly may have increased cerebral blood flow and a greater number of small blood vessels in the brain, researchers here said.

This could be the mechanism by which exercise prevents cognitive decline in the elderly, Feraz Rahman, M.S., a medical student at Jefferson Medical College in Philadelphia, told attendees at the Radiological Society of North America meeting.

"Aerobic exercise improves cognitive function … and counteracts the effects of aging on the brain," Rahman said. "That may be due to blood flow and vasculature."

Previous research has shown that exercise reverses small vessel disease elsewhere in the body, and increases brain volume and cognitive function in the elderly.

Rahman concluded that the findings of this study show that "exercise is a vital part of healthy aging and might slow the loss of small vessels."

MedPage Today

When Peter Nicholson’s mother suffered a series of strokes last winter, he did something women have done for generations: he quit his job and moved into her West Hollywood home to care for her full time.

Mr. Nicholson, 53, is part of a growing number of men who are providing primary care for their aging parents, usually their mothers.

The Alzheimer’s Association and the National Alliance for Caregiving estimate that men make up nearly 40 percent of family care providers now, up from 19 percent in a 1996 study by the Alzheimer’s Association. About 17 million men are caring for an adult.

“It used to be that when men said, ‘I’ll always take care of my mother,’ it meant, ‘My wife will always take care of my mother,’ ” said Carol Levine, director of the families and health care project at the United Hospital Fund. “But now, more and more men are doing it.”

Often they are overshadowed by their female counterparts and faced with employers, friends, support organizations and sometimes even parents who view caregiving as an essentially female role. Male caregivers are more likely to say they feel unprepared for the role and become socially isolated, and less likely to ask for help.

Women still provide the bulk of family care, especially intimate tasks like bathing and dressing. At support groups, which are predominantly made up of women, many women complain that their brothers are treated like heroes just for showing up.

But with smaller families and more women working full-time, many men have no choice but to take on roles that would have been alien to their fathers. Just as fatherhood became more hands-on in the baby boom generation, so has the role for many sons as their generation’s parents age.

And then there is the inevitable question: What happens when I have to bathe her?

“That’s where the rubber meets the road,” said Donna Wagner, the director of gerontology at Towson University and one of the few researchers who has studied sons as caregivers.

Though he is not squeamish about it, he said: “The weirdness permeates our relationship. She doesn’t know if I’m her husband or her boyfriend or her neighbor. She knows she trusts me. But there are times when it’s very difficult. I need to keep her from embarrassing herself. She’ll say things like, ‘I adore you.’ I don’t know who she’s loving, because she doesn’t know who I am. Maybe I’m embarrassed about it — it’s my mom, for Christ sakes. But it’s weird how the oldest son becomes the spouse.”

On a recent evening, Mr. Kassin visited his mother, Doris Golden, in her Manhattan apartment. Ms. Golden, 82, is in the early stages of Alzheimer’s and still lives independently, but relies on Mr. Kassin to arrange her schedule, pay her bills and make sure she remembers her daily tasks (his sister also helps).

In past generations, men might have answered this question by pointing to their accomplishments as breadwinners or fathers. Now, some men say they worry about the conflict between caring for their parents and these other roles.

In a 2003 study at three Fortune 500 companies, Dr. Wagner found that men were less likely to use employee-assistance programs for caregivers because they feared it would be held against them.

“Even though the company has endorsed the program, your supervisors may have a different opinion,” Dr. Wagner said. “I had a man who worked for a large company with very generous benefits, and he was told that if he took more time to go with his dad to chemotherapy, he was at risk of losing his job. He ended up not going with his father.”

Mr. Kassin said that although his employer had been understanding, he was reluctant to talk about his caregiving because “I think it would be looked at like, when they hire a male, they expect him to be 100-percent focused.”

“Nursing homes have a very difficult time dealing with male caregivers,” Ms. Torres said. “It’s unusual for them. The male caregiver is made to feel their interest in their relative is inappropriate. Our male callers say they’re made to feel what they’re doing is unusual, that it’s wrong.”

She gave the example of a son who was the health care agent for his mother and wanted to be in the room when the staff changed her diaper because he was concerned about her skin condition. “The staff refused to allow it,” Ms. Torres said. “They said the mother’s dignity was at risk.”

After two weeks of pressing, she said, he finally got his way. With a daughter, this would not have been an issue, Ms. Torres said.

And even when they are acknowledged, for many male caregivers, as for women, there is the lingering sense that whatever they do is not enough.

“I don’t know if this is just the musings of someone who’s on the verge of tossing everything and putting her in a home,” he said. “But this is a very revealing journey about who I am to me and my family, and what’s important to me.”

The New York Times

A new Israeli device the ReWalk -- worn like an exoskeleton and maneuvered with crutches -- promises to give mobility to paraplegics. The company developing it, Argo Medical Technologies, has made news that has circled the globe.

Cancer researchers have known for years that it was possible in rare cases for some cancers to go away on their own. There were occasional instances of melanomas and kidney cancers that just vanished. And neuroblastoma, a very rare childhood tumor, can go away without treatment.
The New York Times

Danish researchers have found that statins, the drugs widely used to control cholesterol, may have another beneficial effect: lowering the risk of death from pneumonia.
The New York Times

Older adults whose parents lived 100 years or longer are healthier than others their age and have dramatically lower risks of heart attack, stroke, diabetes or dying from any other cause, researchers at the Boston University School of Medicine report in a new study.
The New York Times

Medicare patients started on a thiazolidinedione for diabetes had a higher mortality rate and were more likely to develop congestive heart failure if given rosiglitazone (Avandia) than pioglitazone (Actos), researchers here reported.
MedPage Today

Medical expert: Glenn Smith, Ph.D.
Total time: 0:07:52 minutes

TheMayoClinic.com - Podcast

Author Sara Davidson talks to two medical scientists about how the body ages and the research on trying to extend our healthy life span.
The New York Times - Magazine - Video interview

This morning’s WSJ tells the story of Brian Kammerer who developed Alzheimer’s in his 40s, and the toll the illness takes on him and his family.

Early on, the CFO for a hedge fund forgets what a stapler is and calls his wife from the bathroom for help identifying it. He winds up unemployed. He stops driving.

Even now, at 51, his math skills remain sharp, but he has trouble recognizing neighbors he has known for two decades. Sometimes, he takes a cab to a nearby golf course without telling anyone and hitches a ride back from a stranger, says his wife, Kathy.

Some half a million Americans are living with early-onset Alzheimer’s, the WSJ says. An explainer from the federal Agency for Health Research and Quality gives some signs that go beyond basic loss of short-term memory:

• Problems finding or saying the right word.
• Inability to recognize objects.
• Forgetting how to use simple, ordinary things, such as a pencil.
• Forgetting to turn off the stove, close windows, or lock doors.

Now, just because you have occasional lapses — forgetting a name, leaving a window open — it doesn’t mean you have Alzheimer’s.

And, AHRQ reminds us, many cases of dementia aren’t Alzheimer’s. Often, they’re caused by factors that can be modified, such as depression, alcohol, or medication.

WSJ reporter Shirley Wang talks with Kathy Kammerer about the warning signs for her husband’s Alzheimer’s in this podcast.

The Wall Street Journal

Early-Onset Sufferers Juggle Children, Job and Dementia

Brian Kammerer, the 45-year-old chief financial officer of a small hedge fund, called his wife one day from a cellphone in the men's room of his Manhattan office building. A colleague had just asked him for something, he whispered, but he had no idea what it was.

"It clicks and it holds papers together," he said.

"A stapler?" Kathy Kammerer asked.

"I think that's what it's called," he replied.

Soon after that exchange in early 2003, the father of three was diagnosed with Alzheimer's disease, capping nearly five years of uncertainty and fear about his increasing forgetfulness and difficulty with language.

While most people who get Alzheimer's are over 65, Mr. Kammerer is one of about 500,000 Americans living with Alzheimer's or other dementias at an atypically young age. Alzheimer's takes a long time to develop -- usually, it isn't diagnosed until 10 years after the first symptoms appear -- but more Americans are identifying it early, thanks in part to aggressive screening programs pushed in recent years by groups including the Alzheimer's Foundation of America, a national alliance of caregivers.

The disease can be especially torturous when it creeps up on those in their 30s and 40s. As these patients move through Alzheimer's early stages, they are forced to cope with the dread of not knowing what is happening to them, often in the years when they're raising young children and building financial security. As the disease progresses, there are slip-ups to cover, appearances to keep up. When these "early onset" Alzheimer's sufferers are finally diagnosed, they face hard questions -- whom to tell and when, and what these divulgences mean for their jobs and health insurance.

There are no Alzheimer's cures now on the market. Current medications mitigate some symptoms but don't slow or halt the disease's progression. Pharmaceutical companies are working on new therapies that reduce or remove amyloid, a sticky substance in the brain thought to play a role in the disease. There are more medicines in development for Alzheimer's than any other neurologic disease except pain, according to Pharmaceutical Research and Manufacturers of America, the industry trade group. It will likely be years before a new generation of drugs makes it to market.

Now 51 years old, Mr. Kammerer, like many Alzheimer's patients, had no history of the disease in his family. He grew up on the north shore of Long Island, where he stood out at school for his talent with numbers. After attending college at the State University of New York-Albany, he got a job on Wall Street.

The Wall Street Journal

In Brief:

Heart attack and heart failure patients have a higher risk of a second heart attack or death if they take painkillers, including the generic drug ibuprofen and Celebrex, made by Pfizer, a Danish study has found.

Patients who had suffered a heart attack and were taking Vioxx, a painkiller that has been withdrawn from the market, had 2.7 times the risk of having another heart attack or dying compared with patients not taking painkillers, according to research presented Tuesday at the American Heart Association meeting in New Orleans. Patients taking Celebrex had double the risk; patients taking the generic diclofenac had 1.9 times the risk, and those taking ibuprofen had 1.3 times the risk, the study found.

Based on the findings, doctors should avoid prescribing nonsteroidal anti-inflammatory drugs for these patients, or give them at low doses, a researcher said.

Also Tuesday, researchers said that the risk of heart attacks and strokes for heart-stent patients taking the anti-clotting drug Plavix increased if they also took anti-ulcer medicines like Nexium.

Doctors implant about two million stents a year and often prescribe blood thinners like Plavix, made by Bristol-Myers Squibb and Sanofi-Aventis, to avoid clots. But the drugs raise the risk of stomach bleeding, so they also prescribe Nexium, made by AstraZeneca, or a rival drug in a group known as proton pump inhibitors. About a third of these patients suffered complications within a year, the study said.

The New York Times

Japanese researchers said Thursday they had created functioning human brain tissues from stem cells, a world first that has raised new hopes for the treatment of disease. Stem cells taken from human embryos have been used to form tissues of the cerebral cortex, the supreme control tower of the brain, according to researchers at the government-backed research institute Riken.

The research was led by Yoshiki Sasai at Riken Center for Development Biology in Kobe.

The tissues self-organized into four distinct zones very similar to the structure seen in human fetuses, and conducted neuro-activity such as transmitting electrical signals, the institute said.

Research on stem cells is seen as having the potential to save lives by helping to find cures for diseases such as cancer and diabetes or to replace damaged cells, tissues and organs.

The team’s previous studies showed stem cells differentiated into distinct cells but until now they had never organized into functioning tissues.

“In regenerative therapy, only a limited number of diseases can be cured with simple cell transplants. Transplanting tissues could raise hopes for greater functional recovery,” the institute said in a statement.

“Cultivated tissues are still insufficient and too small to be used to treat stroke patients. But study of in-vitro cultivation of more mature cortex tissues, such as those with six zones like in the adult human brain, will be stepped up,” it said.

The tissues could also serve as “a mini organ” for use in studying the cause of the Alzheimer’s disease and developing vaccines, it said.

Embryonic stem cells are harvested by destroying a viable embryo, a process that some people find unacceptable.

Riken said cortex tissues were also obtained from “induced pluripotent stem cells,” which are similar to embryonic stem cells but artificially induced, typically from adult cells such as skin cells. The cultivated tissues look like miniature mushrooms two millimeters in diameter.

The team also succeeded in making cortex tissues from the embryonic stem cells of mice. Using mouse tissues, scientists confirmed they had formed a network of neurons that properly respond to stimulus.

The tissues can also be selectively induced to different cortex types controlling memories, visual sensation and other tasks.

The findings of the study were published in the Nov 6 online journal Cell Stem Cell in the United States.

Japan Today

PHILADELPHIA, Nov. 4 -- For patients with early age-related macular degeneration, impaired night vision is a risk factor for progression to advanced disease, researchers here found.

The worst scores on an assessment of night vision were significantly associated with a drop in visual acuity and development of choroidal neovascularization and geographic atrophy through follow-up of at least five years, Gui-shuang Ying, Ph.D., of the University of Pennsylvania here, and colleagues reported in the November issue of Ophthalmology.

The associations remained significant after adjusting for baseline participant and ocular characteristics and established risk factors.

"Because of the ease of ascertainment compared with testing dark adaptation or rod sensitivity," the researchers said, "assessing night vision symptoms may be useful in identifying patients with early or intermediate age-related macular degeneration who are at a relatively high risk of progression."

"These results are consistent with the biological and psychological findings that rod photoreceptor degeneration precedes cone degeneration in early age-related macular degeneration, and that rod dysfunction may contribute to the later degeneration of cones because of their interdependence," the researchers said.

The results also implied that different pathophysiological processes resulted in choroidal neovascularization and geographic atrophy because of differences in their associations with night vision symptoms, they said.

In addition to providing independent predictive information about the progression of disease, the researchers said, measuring night vision symptoms may help identify patients for use in clinical trials evaluating agents for the prevention of geographic atrophy.

"Including only patients with night vision symptoms, and therefore higher risk of progression and loss of vision," they said, "would be one way to decrease the risk-benefit ratio in these clinical trials and to decrease the total sample size or follow-up period required to attain a specific amount of statistical power."

MEDPAGE TODAY

NEW HAVEN, Conn., Nov. 4 -- Patients 65 and older may fare better when they are brought into the decision-making of complex treatment trade-offs, researchers here said.

When patients with multiple medical conditions weighed outcomes of treatment options against one another, they typically preferred those that would achieve the outcome they most desired, Terri Fried, M.D., of Yale, and colleagues reported in the October issue of the Journal of the American Geriatrics Society.

"Prioritizing across all outcomes can help clarify what is most important to seniors who are faced with complex healthcare decisions," Dr. Fried said.

About 65% of older Medicare beneficiaries have at least two chronic conditions, and 24% have four or more, the researchers said. These patients often face complex care decisions when the treatment for one condition could worsen another -- which the researchers call "competing outcomes."

For example, if a patient with high blood pressure, heart disease, and osteoarthritis finds that the hypertension medication causes leg cramps that preclude the pool exercises needed to keep the arthritis symptoms in check, the patient may elect to stop taking it.

"I have high cholesterol," one participant said. "I took something but … I had such pain in my calf, so I was taken off whatever that was. I think [my cholesterol] is 241, and I'm willing to live with that."

Many participants initially thought of outcomes in terms of disease-specific goals, such as prevention of a stroke or heart attack. But during the discussions, they changed their focus to more global outcomes, such as quality of life, the researchers said.

For example, some participants, when debating taking a medication that would increase their risk of heart attack in order to treat pain, defined thresholds of decreased function at which they would become willing to take on a greater risk of cardiovascular mortality.

"When participants thought about outcomes in these global terms, they were able to weigh these more general outcomes against one another, in order to reflect on what was most important to them," the researchers wrote.

The researchers said that asking patients to prioritize their desired outcomes would enable physicians to subsequently determine a course of care that would most likely meet their priorities.

They said their study can only be used to "understand how older persons with coexisting conditions think about their illnesses and interventions and not to draw conclusions about their knowledge or perceptions."

However, they said, their findings suggest that asking older patients "to prioritize a set of global outcomes that can be applied across a spectrum of specific diseases may be one easily understood approach to eliciting values in a manner that can inform a range of healthcare decisions."

MEDPAGE TODAY

A 3-year longitudinal study

Objective: To investigate longitudinal change in the medical decision-making capacity (MDC) of patients with amnestic mild cognitive impairment (MCI) under different consent standards.

NEUROLOGY 2008;71:1474-1480

A multiethnic, population-based study of incident cases

Objective: To describe factors associated with survival in Alzheimer disease (AD) in a multiethnic, population-based longitudinal study.

NEUROLOGY 2008;71:1489-1495

Here, the age-adjusted Alzheimer's disease mortality rate in Puerto Rico and United States from 1999 to 2004 was analyzed...

PubMed - Am J Alzheimers Dis Other Demen. 2008 Oct-Nov;23(5):462-9.

CLICK HERE TO READ THE FULL ABSTRACT & LINKS TO RELATED ARTICLES

This review will discuss the possibility that sex hormone binding globulin (SHBG) plays an active role in the aging process.

PubMed - Horm Metab Res. 2008 Oct 27. [Epub ahead of print]
CLICK HERE TO READ THE FULL ABSTRACT & LINKS TO RELATED ARTICLES

Aims: Cube copying measures visuospatial ability, which is often impaired in Alzheimer's disease (AD). Cube copying was examined as an evaluation of cholinesterase inhibitor (ChEI) treatment in AD.

PubMed - Am J Alzheimers Dis Other Demen. 2008 Oct-Nov;23(5):439-46
CLICK HERE TO READ THE FULL ABSTRACT & LINKS TO RELATED ARTICLES

This article describes a model of dementia care in which individual care needs are addressed and the social environment is valued as an essential element in care considerations.

PubMed - Am J Alzheimers Dis Other Demen. 2008 Oct-Nov;23(5):430-8.
CLICK HERE TO READ THE FULL ABSTRACT & LINKS TO RELATED ARTICLES

Depression is common in patients with neurologic disorders such as Alzheimer disease, stroke, Parkinson disease, and multiple sclerosis. Diagnosing depression in the context of neurologic disease is challenging, given the overlap between many signs and symptoms of depression with those of the neurologic disorders.

PubMed - Am J Med. 2008 Nov;121(11S2):S28-S37.
CLICK HERE TO READ THE FULL ABSTRACT & LINKS TO RELATED ARTICLES

Dr. Cheryl Woodson, you may recall from last week’s post, is a seasoned geriatrician in Chicago Heights, Ill., who has found that she can no longer afford to accept new Medicare patients.

Here’s some of Dr. Woodson’s advice on navigating the caregiving maze, which I culled both from her book, “To Survive Caregiving,” and from observing her during a recent day-long visit to her office.

1. Assisted living, a popular solution for elderly people who cannot live independently, is a “myth,” Dr. Woodson said, “a place for people who don’t exist.” Families often believe these facilities will meet all of their loved ones’ needs, enabling caregivers to focus on jobs and family, only to find this isn’t the case.

2. Squaring a family’s expectations with those legal limits would require a thorough, first-hand assessment of the elderly person’s physical and cognitive health before admission to an assisted living facility. That rarely happens. New residents are admitted based on a report from their current physicians, who may not be qualified to diagnose the early signs of dementia and impending immobility or may sugarcoat the situation in order to help a desperate family.

3. Instead, without verifying the physician’s report or the family’s representations, these facilities may admit residents who already need help with simple tasks like dressing or eating, or will in the very near future, and then charge extra for these services.

4. Coordinating all the services that the assisted living facility doesn’t provide generally falls to one sibling, Dr. Woodson noted, who then becomes overwhelmed, sacrificing more than should be expected. The solution is hiring a geriatric care manager — “They should be called rent-a-daughters,” Dr. Woodson said — adding further to the expense, until the resident and family can no longer afford this kind of accommodation and are forced to consider a nursing home.

5. Most families balk at the prospect of transferring an aging parent to a nursing home because they like the aesthetics of assisted living — the carpeted floors, overstuffed chairs and crystal chandeliers.

6. The doctors who see residents at assisted living facilities are essentially freelancers, not employees, since their fees are paid by Medicare and they also may maintain private practices. So rather than hang around the facility expecting them to answer your questions on the fly, Dr. Woodson suggested calling and arranging to see them “by appointment, not by ambush.”

7. If a parent lives in an assisted living facility, families should closely monitor the monthly pharmacy bill, less for cost than for content. Is Xanax being prescribed for anxiety? There are numerous other remedies available without the potentially dangerous side effects. What about muscle relaxants for arthritic pain? They increase confusion in the elderly and add to the risk of falls; instead, ask for pain medication and/or a heating pad. If the assisted living facility offers to have prescriptions filled and delivered by a local pharmacy — a huge convenience for family members — be sure it’s a pharmacy that insists upon periodic blood work or other tests for drugs that are supposed to be closely monitored.

8. The goal of medical care for the elderly, in Dr. Woodson’s view and the view of every geriatrician I’ve ever interviewed, is to make day-to-day life more comfortable, not to cure illness or extend longevity.

9. Apply similar standards to immunizations and vaccinations. If someone is so ill or disabled that death would be welcome, refuse the vaccine for pneumonia, long known as “the old person’s friend.” But never say no to the shingles vaccine, which can prevent an excruciating rash. “Even if someone was only going to live five more minutes, that’s the one thing I’d suggest,” Dr. Woodson says. “It’s a quality-of-life issue.”

10. Do not assume that the presenting symptom of Alzheimer’s disease will be forgetting words, losing things or other obvious examples of short-term memory loss. Often the first thing a family member will notice is an empty checking account, Dr. Woodson said, because a normally cautious and frugal person has been tricked by a get-rich-quick scheme or other scam. And like missing money, look out for pills missing from those seven-day dispensers that help people with multiple medications keep track of what they’re taking and when.

The New York Times
CLICK HERE TO READ THE FULL ARTICLE

Many of you take exception to the notion, expressed here last week by Dr. Cheryl Woodson, that assisted living is a “myth” that promises more than it can deliver to the frail elderly and their families. Interestingly, Dr. Woodson’s provocative observation is echoed in a study and an editorial in the current issue of the Journal of the American Medical Directors Association, both of which suggest that the medical needs of many current assisted-living residents exceed what these facilities can provide and that consumers are not adequately warned of these limitations.

Dr. Matthew K. McNabney, a geriatrician and assistant professor of medicine at Johns Hopkins University, and his fellow researchers reviewed the medical charts of 198 residents at 22 assisted living facilities in central Maryland, then interviewed those residents, their family members and the facility staff. They found that 46 percent of the residents had chronic conditions in three or more broad disease categories, such as those affecting the cardiovascular, pulmonary or endocrine systems. In addition, 25 percent had two or more specific diagnoses, such as congestive heart failure, osteoporosis or Parkinson’s disease, covered by clinical guidelines in use at long-term care facilities.

“As with nursing homes, many assisted living facilities perform admirably,” he wrote in the editorial. “However, overall performance across the country is uneven and often problematic. The public is still not getting a balanced picture of the variability, capabilities and limitations of assisted living. The AL propaganda machine often makes it difficult to engage in a meaningful discussion about reality. Instead, it often shouts down such discourse with the usual platitudes.”

“What almost certainly is needed in the long term,” Dr. McNabney added, “is not pretty decorations, but the capacity and commitment to care for people as their needs progress.”

There are two models of long-term care that experts say more realistically acknowledge the inevitability of decline and dependence among the elderly: CCRCs, or continuing care retirement communities, which require large up-front expenditures as well as high monthly fees; and PACE, an acronym for “program of all-inclusive care for the elderly,” a joint venture of Medicare and Medicaid that operates 42 programs in 22 states and serves low-income clients. We’ll be talking more about them in the future.

The New York Times

CLICK HERE TO READ THE FULL ARTICLE

BACKGROUND: Subjects with Alzheimer's disease (AD) have elevated cortisol levels as a result of hypothalamic-pituitary-adrenal (HPA) axis dysfunction. Acute administration of hydrocortisone has been associated with working memory (WM) performance in young adults.

PubMed - Arq Neuropsiquiatr. 2008;66(3b):619-624.
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

BACKGROUND: Disclosure of the diagnosis of Alzheimer's disease (AD) remains a contentious issue, and has been little studied in developing countries.

PubMed - Arq Neuropsiquiatr. 2008;66(3b):625-630.
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

This study evaluated the benefits of a Psychoeducational Intervention Program (PIP) on caregiver burden in southern Europe.

PubMed - Int J Geriatr Psychiatry. 2008 Oct 23. [Epub ahead of print]
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

This review discusses the utility of transgenic mice as a research tool and their contributions to our understanding of Alzheimer disease.

PubMed - J Biol Chem. 2008 Oct 22. [Epub ahead of print]
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

This video article takes the form of a debate between Dr. Morgan and Dr. Landreth on the merits and drawbacks of an Alzheimer's disease vaccine. Click on Supplemental Material to watch the streaming video.

PubMed - J Neuroimmune Pharmacol. 2008 Oct 23. [Epub ahead of print]
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

Background/Aims: To examine the incremental effect of patients' dependence on others, on cost of medical and nonmedical care, and on informal caregiving hours over time.

PubMed - Dement Geriatr Cogn Disord. 2008 Oct 22;26(5):416-423. [Epub ahead of print]
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

Autopsy cases who had received Abeta vaccine showed clearance of senile plaques, and beneficial effect was shown in patients who had high antibody titers to amyloid plaques. Thus, vaccination is widely accepted as promising therapy for Alzheimer disease.

PubMed - Nippon Rinsho. 2008 Oct;66(10):2008-12.
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

In this review we have summarized current proteomics technologies involved in discovery of biomarkers for neurodegenerative diseases, practical considerations and limitations of several major aspects, as well as the current status of candidate biomarkers revealed by proteomics for Alzheimer and Parkinson disease.

PMID: 18938247 [PubMed - as supplied by publisher]
PubMed - Neurobiol Dis. 2008 Sep 26. [Epub ahead of print]
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

OBJECTIVES: To evaluate the prevalence of white-coat effect (WCE), and its association with individual anxiety and insight of disease, among older patients evaluated for suspected cognitive impairment.

PMID: 18937278 [PubMed - as supplied by publisher]
PubMed - Int J Geriatr Psychiatry. 2008 Oct 20. [Epub ahead of print]
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

OBJECTIVE: This study explored how male and female family caregivers of Alzheimer's disease (AD) patients differ in their use of formal services and informal support and how religiousness may affect such differences.

PMID: 18936242 [PubMed - as supplied by publisher]
PubMed - J Aging Health. 2008 Oct 20. [Epub ahead of print]
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

BACKGROUND: There is evidence of increased systemic expression of active GSK3B in Alzheimer's disease patients, which apparently is associated with the formation of senile plaques and neurofibrillary tangles.

PMID: 18932008 [PubMed - as supplied by publisher]
PubMed - Eur Arch Psychiatry Clin Neurosci. 2008 Oct 17. [Epub ahead of print]
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

The objective of this study was to determine the relationship between cognitive performance and plasma levels of tHcy and its biological determinants folate and vitamin B(12), and lipids in clinically diagnosed AD patients.

PMID: 18931498 [PubMed - as supplied by publisher]
PubMed - Dement Geriatr Cogn Disord. 2008 Oct 16;26(4):384-390. [Epub ahead of print]
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

Objectives: There exists little information describing the spectrum and correlations of sexual behaviors manifested by elders with dementia living in residential care.

PMID: 18931496 [PubMed - as supplied by publisher]
PubMed - Dement Geriatr Cogn Disord. 2008 Oct 16;26(4):370-377. [Epub ahead of print]
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

BACKGROUND: Cross-sectional reports suggest that statin-users are less likely to have Alzheimer disease (AD). Prospective studies have provided inconsistent evidence.

PubMed - J Neurol Neurosurg Psychiatry. 2008 Oct 17. [Epub ahead of print]
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

This article provides an update of the available drug therapies for AD and discusses their implications on the oral and dental health of patients.

PubMed - Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2008 Oct;106(4):467-76
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

This review will focus also on particular classes of AChEIs, namely dual binding site AChEIs, which are being purposely designed to target Abeta aggregation and / or other biological targets that contribute to AD pathogenesis, thus constituting very promising disease-modifying anti-Alzheimer drug candidates.

PubMed - Curr Med Chem. 2008;15(24):2433-55.
CLICK HERE TO READ FULL ABSTRACT & LINKS TO RELATED INFORMATION

PHILADELPHIA — Antonio Vasquez was just 60 when Alzheimer’s disease derailed him.

He lost his job at a Queens bakery because he kept burning chocolate chip cookies, forgetting he had put them in the oven. Then he got lost going to job interviews, walking his neighborhood in circles.

Teresa Mojica of Philadelphia was 59 when she got Alzheimer’s, making her so argumentative and delusional that she sometimes hits her husband. And Ida J. Lawrence was 57 when she started misplacing things and making mistakes in her Boston dental school job.

Besides being young Alzheimer’s patients — most Americans who develop it are at least 65, and it becomes more common among people in their 70s or 80s — the three are Hispanic, a group that Alzheimer’s doctors are increasingly concerned about, and not just because it is the country’s largest, fastest-growing minority.

Studies suggest that many Hispanics may have more risk factors for developing dementia than other groups, and a significant number appear to be getting Alzheimer’s earlier. And surveys indicate that Latinos, less likely to see doctors because of financial and language barriers, more often mistake dementia symptoms for normal aging, delaying diagnosis.

“This is the tip of the iceberg of a huge public health challenge,” said Yanira L. Cruz, president of the National Hispanic Council on Aging. “We really need to do more research in this population to really understand why is it that we’re developing these conditions much earlier.”

It is not that Hispanics are more genetically predisposed to Alzheimer’s, say experts, who say the diversity of ethnicities that make up Hispanics or Latinos make a genetic explanation unlikely.

Rather, experts say several factors, many linked to low income or cultural dislocation, may put Hispanics at greater risk for dementia, including higher rates of diabetes, obesity, cardiovascular disease, stroke and possibly hypertension.

The New York Times
CLICK HERE TO READ THE FULL ARTICLE

MedPage TodayMILAN, Oct. 20 -- More education and mentally challenging employment appear to protect against the cognitive impairment of Alzheimer's disease, researchers here said.

The findings appear to confirm the so-called "brain reserve hypothesis," which suggests that high intelligence, education, and an active lifestyle are associated with a reserve capacity that protects the brain against the effects of aging and disease, according to Valentina Garibotto, M.D., of the Italian National Institute of Neuroscience, and colleagues.

But it remains unclear whether the reserve is a genetic endowment that also leads to higher education and employment or whether such mental challenges create the reserve, Dr. Garibotto and colleagues said in the Oct. 21 issue of Neurology.

"The theory is that education and demanding jobs create a buffer against the effects of dementia on the brain, or a cognitive reserve," Dr. Garibotto said.

For people with such a history, "their brains are able to compensate for the damage and allow them to maintain functioning in spite of damage," she said.

Indeed, in the study, people with more education and more demanding jobs tended to have more brain damage for a given level of impairment -- indicating, the researchers said, that they cope better with the disease than their less educated counterparts.

On the other hand, among the probable Alzheimer's patients, higher educational level was associated -- for the same level of clinical impairment -- with lower blood glucose in the right temporo-parietal association cortex and the precuneus. The association was significant at P<0.01.>

There are two possible explanations of the findings, Dr. Garibotto said.

"The brain could be made stronger through education and occupational challenges," she said, "or genetic factors that enabled people to achieve higher education and occupational achievement might determine the amount of brain reserve."

But, she added, it isn't possible yet to say which explanation holds true.

MedPage Today

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White matter hyperintensities (WMH) are frequently seen on T(2)-weighted MRI scans of elderly subjects with and without Alzheimer's disease.

Brain. 2008 Oct 16. [Epub ahead of print]
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Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, USA.

Alzheimer disease (AD) is the most common cause of dementia in adults. The current therapy for AD has only moderate efficacy in controlling symptoms, and it does not cure the disease. Recent studies have suggested that abnormal hyperphosphorylation of tau in the brain plays a vital role in the molecular pathogenesis of AD and in neurodegeneration. This article reviews the current advances in understanding of tau protein, regulation of tau phosphorylation, and the role of its abnormal hyperphosphorylation in neurofibrillary degeneration.

PMID: 18855662 [PubMed - in process]
Curr Med Chem. 2008;15(23):2321-8.
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Laboratori de Química Farmacèutica (Unitat Associada al CSIC), Facultat de Farmàcia, Universitat de Barcelona, Av.

The therapeutic arsenal for the treatment of Alzheimer's disease (AD) remains confined to a group of four inhibitors of AChE and one NMDA receptor antagonist, which are used to provide a relief of the very late symptoms of the dementia, i.e. the cognitive and functional decline.....

This review will focus also on particular classes of AChEIs, namely dual binding site AChEIs, which are being purposely designed to target Abeta aggregation and / or other biological targets that contribute to AD pathogenesis, thus constituting very promising disease-modifying anti-Alzheimer drug candidates.

PMID: 18855672 [PubMed - in process]
Curr Med Chem. 2008;15(24):2433-55
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Wolfson Centre for Age-Related Diseases, Guy's Campus, King's College London.

Neuropsychiatric symptoms are frequent in people with dementia, result in distress for the people experiencing them and their caregivers, and are a common precipitant of institutional care. The safe and effective treatment of these symptoms is a key clinical priority, but is a long way from being achieved. Psychological interventions are recommended as the first line treatment strategy in most good practice guidelines, and there is emerging evidence of efficacy for agitation and depression.

PMID: 18925489 [PubMed - in process]
Int Rev Psychiatry. 2008 Aug;20(4):396-404.
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SAN DIEGO, Oct. 14 -- High-dose vitamin B supplements reduced homocysteine levels but did not slow Alzheimer's disease progression, researchers here found in a large placebo-controlled trial.

After 18 months of treatment, patients taking high doses of vitamins B6 and B12 as well as folic acid showed the same degree of cognitive decline compared with baseline as those assigned to placebo, reported Paul Aisen, M.D., of the University of California San Diego, and colleagues in the Oct. 15 issue of the Journal of the American Medical Association.

Participants in the vitamin group also showed a significantly higher frequency of depressive symptoms, seen in 27.9% compared with 17.8% of the placebo group (P=0.02). Blurred vision and hyperhidrosis also appeared more common with vitamin supplements, but the differences missed statistical significance (P=0.7 and 0.53, respectively).

"Our study does not support the treatment of individuals with mild to moderate Alzheimer's disease and normal vitamin levels with B vitamin supplements," Dr. Aisen and colleagues concluded.

The study was prompted by earlier findings that blood homocysteine levels are elevated in patients with Alzheimer's disease and that B vitamin supplements can lower homocysteine levels.

But there was not even a hint that vitamin supplements slowed participants' cognitive decline by any measure used in the study:

--Alzheimer Disease Assessment Scale cognition scores increased 6.54 points (SD 8.17) in the placebo group after 18 months, compared with 7.38 points (SD 9.72) in the vitamin supplement group.

--Mini-Mental State Exam scores decreased 3.08 points (SD 4.46) in the placebo group versus 2.65 points (SD 4.56) with supplements.

--Clinical Dementia Rating scores increased 2.51 points (SD 2.57) with placebo compared with 2.58 points (SD 2.45) in the supplement group.

--Activities of daily living scores on the Alzheimer Disease Cooperative Study index decreased 10.00 points (SD 11.09) with placebo versus 10.96 points (SD 12.36) with supplements.

Dr. Aisen and colleagues stopped short of ruling out any benefit from vitamin B supplements for anyone.

"Randomized studies in individuals without dementia have yielded conflicting results; supplementation may be useful in older individuals with relatively high homocysteine levels," they wrote. "The identification of groups that may benefit from such treatment remains an important goal."

They said it was possible that supplements might be more effective if begun while cognition is still intact. "Individuals with established cognitive impairment may be refractory to treatment," Drs. Clarke and Bennett suggested.

But until future research identifies populations or circumstances in which supplements are beneficial, "there is insufficient evidence to justify routine use of homocysteine-lowering vitamin supplements for the prevention of Alzheimer disease and cognitive decline among individuals with normal vitamin status," they said.

MedPage Today
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Laboratori de Química Farmacèutica (Unitat Associada al CSIC), Facultat de Farmàcia, and Institut de Biomedicina (IBUB), Universitat de Barcelona, Av. Diagonal 643, E-08028-Barcelona, Spain.

The therapeutic arsenal for the treatment of Alzheimer's disease (AD) remains confined to a group of four inhibitors of AChE and one NMDA receptor antagonist, which are used to provide a relief of the very late symptoms of the dementia, i.e. the cognitive and functional decline.

This review will focus also on particular classes of AChEIs, namely dual binding site AChEIs, which are being purposely designed to target Abeta aggregation and / or other biological targets that contribute to AD pathogenesis, thus constituting very promising disease-modifying anti-Alzheimer drug candidates.

PMID: 18855672 [PubMed - in process]
PubMed
Curr Med Chem. 2008;15(24):2433-55.
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Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, USA.

Alzheimer disease (AD) is the most common cause of dementia in adults. The current therapy for AD has only moderate efficacy in controlling symptoms, and it does not cure the disease. Recent studies have suggested that abnormal hyperphosphorylation of tau in the brain plays a vital role in the molecular pathogenesis of AD and in neurodegeneration. This article reviews the current advances in understanding of tau protein, regulation of tau phosphorylation, and the role of its abnormal hyperphosphorylation in neurofibrillary degeneration. Furthermore, several therapeutic strategies for treating AD on the basis of the important role of tau hyperphosphorylation in the pathogenesis of the disease are described. These strategies include (1) inhibition of glycogen synthase kinase-3beta (GSK-3beta), cyclin-dependent kinase 5 (cdk5), and other tau kinases; (2) restoration of PP2A activity; and (3) targeting tau O-GlcNAcylation. Development of drugs on the basis of these strategies is likely to lead to disease-modifying therapies for AD.

PMID: 18855662 [PubMed - in process]
PubMed
Curr Med Chem. 2008;15(23):2321-8.
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Przychodnia Chorób Zawodowych Wsi, Instytut Medycyny Wsi, 20-950 Lublin, ul. Jaczewskiego 2.

Patients with dementia, especially with dementia in the course of Alzheimer's disease require long-time care. The aim of the research was to assess how caregivers deal with everyday care problems, especially the psychical and social ones. The study was conducted in 1999 by the method of anonymous inquiry in the group of 42 caregivers, mostly members of Lublin's Alzheimer Association. The caregivers are children (53.6%) or spouses of patients (39.8%). In 61% of cases patient lives with the carer's family. 72% of our respondents consider their work as very hard. The care takes them seven days a week, 77% of carers have no possibility of rest. Almost half of respondents (47%) constantly feel depressed and tired. 15% claim that they hardly cope with nursing. 39% of caregivers have the feeling of deep, internal exhaustion.

PMID: 18853662 [PubMed - in process]
PubMed
Przegl Lek. 2008;65(6):304-7
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Department of Neurology, Emory University School of Medicine, 1841 Clifton Road NE, Atlanta, GA 30329, USA. mevatt@emory.edu

BACKGROUND: A role for vitamin D deficiency in Parkinson disease (PD) has recently been proposed.

CONCLUSIONS: This report of 25(OH)D concentrations in a predominantly white PD cohort demonstrates a significantly higher prevalence of hypovitaminosis in PD vs both healthy controls and patients with AD. These data support a possible role of vitamin D insufficiency in PD. Further studies are needed to determine the factors contributing to these differences and elucidate the potential role of vitamin D in pathogenesis and clinical course of PD.

PMID: 18852350 [PubMed - in process]
Arch Neurol. 2008 Oct;65(10):1348-52.
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Department of Neurosciences, University of California, San Diego, 9500 Gilman Dr, M/C 0949, La Jolla, CA 92093, USA. paisen@ucsd.edu

CONTEXT: Blood levels of homocysteine may be increased in Alzheimer disease (AD) and hyperhomocysteinemia may contribute to disease pathophysiology by vascular and direct neurotoxic mechanisms. Even in the absence of vitamin deficiency, homocysteine levels can be reduced by administration of high-dose supplements of folic acid and vitamins B(6) and B(12). Prior studies of B vitamins to reduce homocysteine in AD have not had sufficient size or duration to assess their effect on cognitive decline.

CONCLUSION: This regimen of high-dose B vitamin supplements does not slow cognitive decline in individuals with mild to moderate AD.

PubMed
JAMA. 2008 Oct 15;300(15):1774-83.
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One tiny brain cell is all it takes to restore voluntary movement of paralysed muscles, scientists in the United States reported Wednesday.

In experiments pointing to new treatments for paralysis caused by spinal cord injury or stroke, monkeys learned within minutes to harness the power of a single neuron to activate muscles immobilised by drugs.

There are some 100 billion neurons in the human brain, and the study suggests an unsuspected degree of flexibility in the kinds of tasks they can perform.

"Nearly every neuron we tested could be used to control this type of stimulation," Chet Moritz, lead author and a researcher at the University of Washington, told journalists in a conference call.

If a monkey can do it, a human should be able to do it even better, he said.

Clinical trials, however, are at least several years away, perhaps longer, Moritz added.

Spinal cord injuries cripple hundreds of thousands of people worldwide every year, rendering the simplest of actions -- opening a door, scratching an itch, drinking a glass of water -- frustratingly difficult, or simply impossible.

Those afflicted with the most severe form of paralysis, known as lock-in syndrome, are fully conscious prisoners inside a body that no longer responds to commands.

While the brain activity that would normally result in a voluntary movement is still present, the instructions simply don't reach the muscles.

Moritz and two colleagues at the University of Washington found a way to bypass the kind of nerve damage that can result in such paralysis.

They first connected electrodes to individual neurons inside the motor cortex of monkey's brain and recorded the electrical activity.

These signals were then routed in real-time to a computer, and from there through a stimulator to another set of electrodes attached directly to wrist muscles that had been artificially blocked further up the arm along the normal neural pathway.

Because little processing power is needed, the computer is the size of a cell phone, and can be attached to the animal's body.

Future versions will be wireless and small enough to implant directly in the body, the researchers said.

The monkey had already mastered a simple video game, grasping targets shown on a video screen with a control device manipulated by a single hand.

"But once he was paralysed, the only way to move his wrist was to change the activity of individual neurons in his brain," Moritz explained.

On average it took about 10 minutes for the monkeys to "train" the neuron well enough to play the video game again.

"The brain can very rapidly learn to control new cells and use them to generate movements," said co-author Eberhard Fetz.

Earlier experiments enabling monkeys to manipulate prosthetic devices or computer cursors using only electrical impulses coming from the brain were based on a fundamentally different premise, according to the new study.

"They tried to read the mind of the money and figure out what he was planning to do," a technique that required massive computing power, said Moritz.

"Our approach is to recreate the raw connectivity between single neurons in the brain and muscles, and let the monkey's nervous system learn how to use that connectivity."

This is also the first study to show that a one neuron can control a muscle -- and possibly a whole group of muscles.

Electrodes connected to a single location in the spinal cord below an injury may be able to activate 10 or 15 muscles that are already precisely balanced for, say, grasping a coffee mug or walking, the researchers said.

And if a stroke has damaged the motor cortex, patients might be able to commandeer other brain cells that do not usually play a role in controlling muscles.

Several obstacles remain, however, before this new technique can be tested in humans, he said.

To avoid infections, the system would have to become fully implantable so that no wires passed through the skin. And electrodes would need to be made more stable so that they could record the activity of neurons over a period of years, rather than weeks.

Breitbart.com

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Department of Neurology, Alzheimer Centre, VU University Medical Center, PO Box 7057, De Boelelaan 1118, 1007 MB Amsterdam, Noord Holland, The Netherlands; Department of Clinical Neurophysiology, VU University Medical Centre, PO Box 7057, 1007 MB Amsterdam, The Netherlands.

OBJECTIVE: We examined the relation between Apolipoprotein E epsilon4 allele (ApoE epsilon4) genotype and functional connectivity measured by Electroencephalography (EEG) in patients with Alzheimer's disease (AD) and patients with subjective complaints (SC).

SIGNIFICANCE: The observed increase in SL in both AD and patients with SC carrying ApoE epsilon4 suggests a strong genetic impact of ApoE epsilon4 on brain function.

PMID: 18848805 [PubMed - as supplied by publisher]
Clin Neurophysiol. 2008 Oct 9. [Epub ahead of print]

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From the Department of Psychiatry, University of Pittsburgh School of Medicine, Western Psychiatric Institute and Clinic (AJB, MAD, CFR); and Carnegie Mellon University (VA, JF, SS, HW), Pittsburgh, PA.

The number of older Americans afflicted by Alzheimer disease and related dementias will triple to 13 million persons by 2050, thus greatly increasing healthcare needs. An approach to this emerging crisis is the development and deployment of intelligent assistive technologies that compensate for the specific physical and cognitive deficits of older adults with dementia, and thereby also reduce caregiver burden.

PMID: 18849532 [PubMed - as supplied by publisher]
Am J Geriatr Psychiatry. 2008 Oct 10. [Epub ahead of print]

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Department of Pharmacological and Pharmaceutical SciencesCollege of Pharmacy, University of Houston, Houston, Texas.

BACKGROUND: Alzheimer's disease (AD) is a degenerative disorder that leads to progressive cognitive decline. Alzheimer's disease develops as a result of over-production and aggregation of beta-amyloid (Abeta) peptides in the brain. The reason for variation in the gravity of symptoms among AD patients is unknown and might result from patient-related factors including lifestyle. Individuals suffering from chronic stress are at an increased risk for developing AD. This study investigated the effect of chronic psychosocial stress in Abeta rat model of AD.

CONCLUSIONS: Chronic stress significantly intensified Abeta-induced deficits of short-term memory and E-LTP by a mechanism involving decreased CaMKII activation along with increased calcineurin levels.

PMID: 18849021 [PubMed - as supplied by publisher]
Biol Psychiatry. 2008 Oct 10. [Epub ahead of print]

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Department of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky Academic Medical Center, 511C Pharmacy Building, 725 Rose Street, Lexington, KY 40536-0082, USA; Graduate Center for Toxicology, University of Kentucky Academic Medical Center, Lexington, KY 40536-0305, USA.

The objective was to estimate oral Al bioavailability from tea infusion in the rat, using the tracer (26)Al. (26)Al citrate was injected into tea leaves.

Further testing of the hypothesis that Al contributes to Alzheimer's disease may be more warranted with studies focusing on total average daily food intake, including tea and other foods containing appreciable Al, than drinking water.

PMID: 18848597 [PubMed - as supplied by publisher]
Food Chem Toxicol. 2008 Sep 21. [Epub ahead of print]

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Genetic studies are a critical source of knowledge about neurodegenerative diseases. The identification of families with an autosomal dominant pattern of inheritance has proven crucial in improving our care of patients with conditions such as Alzheimer disease (AD) and Parkinson disease. This work has led to improvements in diagnostic accuracy, a better understanding of the biologic mechanisms underlying disease, and most importantly, the identification of targets for therapeutic intervention. Recently, genetic studies of patients with frontotemporal dementia (FTD) have proven to be very fruitful. Two distinct, genetically determined causes have been defined in the last decade. These include the locus of the gene coding for the microtubule-associated protein tau (MAPT) on chromosome 17,1 and within the last 2 years, the gene coding for progranulin (GRN), also on chromosome 17.2,3

Despite these remarkable advances, the glass remains half empty. Why? There is substantial reason to be optimistic about our ability to identify the cause of FTD in up to 27% of patients with an autosomal dominant family history. However, the cause of disease remains a mystery in 73% of patients with FTD. Many pieces of the puzzle remain to be found. Very few studies have pursued interacting genetic factors, for example, and even fewer studies have examined environmental risk factors for FTD and more complex interactions between genetics and the environment. Much biomarker work is needed to identify the histopathologic abnormalities during life of patients with sporadic FTD who show accumulations of the same aberrant proteins at autopsy. This would allow treatments developed for familial FTD to be administered safely and confidently to patients with similar sporadic diseases.

The report of Seelaar et al. provides us with an important yardstick indicating our remarkable success in identifying the cause of FTD in an impressively large percentage of these patients. They also point us in informative directions for future work that can identify the cause of disease in some additional familial patients with FTD. Before breaking out the champagne, however, we should consider the large amount of work that remains before we can improve the care of all patients with FTD.

Despite many promising leads, new treatments for Alzheimer's are slow to emerge. Future treatments will likely focus on stopping the disease in people at risk.

Alzheimer's treatments consist mainly of medications that stabilize cognitive function, if only for a short period of time. These drugs stage a holding action, primarily postponing further cognitive declines.

But the Alzheimer's treatments of the future will focus more on preventing the disease or halting its progress in its earliest stages. The following treatment options are among the strategies currently being studied.

Alzheimer's vaccine

Immunization can reduce the number of amyloid plaques — clusters of abnormal cells associated with Alzheimer's disease — in the brain. But a human trial of an Alzheimer's vaccine was halted when several participants developed brain inflammation.

Secretase modulators

Secretase-modifying drugs might block the action of the clumping enzymes, or activate the nonclumping enzyme.

Certain anti-inflammatory drugs — including ibuprofen (Advil, Motrin, others), naproxen sodium (Aleve) and indomethacin (Indocin) — appear to modify how one of these enzymes works, so that it doesn't produce fragments that clump. One of the most promising drugs being studied in this group is tarenflurbil (Flurizan).

Antibiotics

A three-month course of antibiotics, specifically doxycycline and rifampin, reduced the rate at which cognitive problems worsened in a group of people who had mild to moderate Alzheimer's disease. The antibiotics appear to interfere with the development of amyloid plaques in the brain.

Hormones

Early studies indicated that hormone replacement therapy, typically prescribed to ease menopausal symptoms, might protect women over the age of 65 against Alzheimer's. But more recent studies not only refute these findings but also suggest that this hormone therapy might even increase the risk of dementia.

In men, low testosterone levels have been linked to increased risk of Alzheimer's disease. Researchers are investigating whether testosterone supplements might help men who have Alzheimer's or are at risk of the disease, but the results have been mixed.

Timeline for answers

New Alzheimer's treatments take time to develop, and then even more studies are needed to establish a treatment's safety and effectiveness. But all this time and effort will eventually pay off. Most researchers expect to see major progress in the treatment and prevention of Alzheimer's in the next few decades.

MayoClinic.com
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Heredity, genetics make disease more likely, but how much isn't clear

For adult children of patients with Alzheimer’s disease, the diagnosis can be devastating — and not just because of what it means for their parents.

Along with concerns about caregiving and grief over the loss of the mother or father they knew, there’s another, more private fear: What if I get it, too?

“I think about it all the time,” said Julie Winokur, 44, a videographer from Montclair, N.J., who chronicled her father’s decline into dementia and its effects on her family. “It’s a terrifying thing to me.”

But even as scientists say they may be getting closer to predicting who may develop the mind-robbing disorder, thanks to new research into biomarkers, heredity and genetics, many children of people who suffer or died from the disease say they wouldn’t want to know.

“My feeling is I’d only want to know if there’s something I can do about it,” said Winokur.

Right now, that’s not the case, Alzheimer’s experts concede. There’s virtually no known cause, no cure and no prevention for the disease that causes memory loss and mental deterioration and affects some 5.2 million people in the U.S. and some 27 million people worldwide.

“I don’t know of anything that has been documented to prevent the onset of this disease,” said Dr. Thomas Bird, a neurologist and Alzheimer's disease researcher at the University of Washington in Seattle. “The advice you get is the advice you’d give to anybody to live a good, healthy lifestyle: Watch your weight, watch your blood pressure, eat a balanced diet.”

Recommendations for ways to predict the disease are even more vague. Perhaps 5 percent of Alzheimer’s cases are caused by a rare genetic mutation responsible for early onset of the disorder that usually strikes after 65. For the rest, scientists have proposed analyzing everything from blood, saliva, skin cells, urine and brain scans to detect early signs of the disorder, with no irrefutable results.

Even the most reliable marker of risk, the apolipoprotein E-e4 gene, known as ApoE4, doesn’t determine for sure whether a person will develop Alzheimer’s. Many people with the gene do get the disease, but many don’t, prompting most experts to advise against screening, Bird said.

That leaves offspring of one or both parents with dementia in limbo, focusing on doing anything they can to stave off Alzheimer’s, even when there’s no clear agreement on what that might be. That can range from working crossword puzzles and gulping antioxidants to engaging in new forms of physical exercise, techniques suggested — but not proven — to prevent the disease.

“We’re being much more vigilant about our exercise,” said Karen Moldt, 54, of the oldest of five siblings in Cary, N.C., who were “shell-shocked” when their father was diagnosed with Alzheimer’s four years ago. “One of my brothers who is right-handed started doing things with his left hand.”

Genetics, heredity boost risk

Still, recent research into genetics and heredity suggests that children like Winokur and Moldt have reason to worry.

Just this summer, Dr. Piero Antuono and a team of scientists at the Medical College of Wisconsin reported that healthy offspring of Alzheimer’s patients who carry the ApoE4 gene show declines in brain function that are detectable long before any clinical symptoms appear.

And last spring, Bird and a team of researchers at the University of Washington revealed that children with two parents who have Alzheimer’s disease are far more likely to get the disease themselves.

In the study of 111 families in which two parents were diagnosed with Alzheimer’s, more than 22 percent of the adult children also developed the disease. That compares to about 13 percent expected in the general population, according to the national Alzheimer's Association. The risk rose with age, affecting 30 percent of children older than 60 and nearly 42 percent of those older than 70.

“I pretty much though that my odds of getting it had to be higher than anybody walking down the street,” said Gayle Dorman, 63, of Tacoma, Wash., a study participant who lost both parents to Alzheimer’s a decade ago.

Increasingly, families like Dorman’s are confronting what neurologist Dr. Daniel I. Kaufer calls the “double-parent dementia dilemma.”

“The way I convey this to children is that it’s a double whammy,” said Kaufer, who directs the Memory and Cognitive Disorders program at the University of North Carolina School of Medicine. “They have the burden of care and the burden of risk.”

‘Oh my god, I hope this doesn't happen to me’
Coping with that burden isn’t easy for family members confronting their own future, said Dr. Zoe Lewis, a palliative care specialist and author of a new book, “I Hope They Know: The Essential Handbook on Alzheimer’s Disease and Care.”

“It is literally the collective fear of anyone, anywhere: Oh my god, I hope this doesn’t happen to me,” Lewis said.

As patients watch their parents spiral downward, often over several years or even decades, they can't help but wonder whether that's the fate they face.

"The fear is that you'll lose your mind and you won't be treated well," Lewis explained.

That fear permeates daily life, making children vigilant for signs of dementia, said Dorman. “For me, it’s pretty scary when I forget where I parked my car. I think, ‘Here it is, here I go.’”

Winokur said she quizzes herself constantly, testing to see whether she remembers people’s names and what they were wearing.

Many children of parents with dementia say they’ve considered confirming their risk by being screened for the ApoE4 gene — and then rejected the idea. “Right now, I don’t know if I’d want to know,” Dorman said.

Others, however, think the information could be valuable. “You could just plan better. If you have a ticking time bomb, you’d want to know, wouldn’t you?” said Mike Sanchez, 37, of Santa Ana, Calif. His 82-year-old father has had Alzheimer’s disease for more than a decade.

Most children of dementia patients are able to put their fear in perspective, said Bird, the University of Washington researcher whose own mother died of Alzheimer's disease.

"I know that I'm at risk for it. Everybody who gets older is at risk. My risk is higher than average," he said. "But I don't feel there's anything more than I could do than I do to prevent it. I don't worry about a disease that I can't prevent."

But at least one son of an Alzheimer’s patient had his worry confirmed in the worst way: By developing signs of the disease himself.

“Within the last nine months, when I try to think of a word, I draw a blank. I’ll know I’m looking for a word and can’t find it,” said Francis, a 59-year-old mechanical engineer from South Carolina who watched his mother succumb to the disease.

He asked to be identified only by his middle name because he hasn’t told his children or his employer that he likely has early-onset Alzheimer’s disease. He has begun taking donepezil, popularly known as Aracept, one of a handful of drugs aimed at slowing cognitive decline.

Francis is clear that he does not want his wife and grown children burdened by his disease. He said he wouldn’t think of asking them to care for him at home if the disease gets worse.

“If it happens to me, I will probably divorce my wife, become indigent and let the government take care of me,” he said.

That’s a stark contrast to Winokur, who said the care she provided keeping her father at home should serve as a model for her children.

“I would really pray that by example, that’s just something you can expect,” she said. “I would definitely want to stay at home. I fulfilled what I would want.”

Researchers like Antuono, who also lost his mother to Alzheimer's, expect to have a reliable treatment for Alzheimer's within a decade.

"In 10 years we'll have an intervention that willl compress the first symptoms of the disease all the way to end," he said, noting that it likely will make the disease a chronic condition, but will not cure the disorder. "A cure to get rid of this altogether? That might be left to the next generation."

ORLANDO, Sept. 27 -- Moderate to severe atrophic vaginitis can be eased for postmenopausal women by either of two low doses of estrogen cream, with no endometrial safety signals, investigators reported here.

Both low-dose regimens of the conjugated estrogen cream led to significant improvement in vaginal maturation index, vaginal pH, and most bothersome symptoms compared with placebo, Gloria Bachmann, M.D., of Robert Wood Johnson Medical School in New Brunswick, N.J., said at the North American Menopause Society meeting.

The improvement was statistically significant at 12 weeks and persisted during follow-up for a year.

In a subgroup of patients who had endometrial biopsies, no cases of endometrial hyperplasia or carcinoma occurred with either estrogen cream regimen.

"Low-dose [vaginal estrogen cream] represents an important therapy for treating atrophic vaginitis without endometrial safety concerns over a one-year study period," Dr. Bachmann and colleagues concluded.

As many as 40% of postmenopausal women are affected by atrophic vaginitis. Vaginal application of topical low-dose estrogens is thought to reduce systemic exposure to estrogen and limit its stimulatory effects on the endometrium, the investigators said.

Both daily and twice-weekly vaginal administration of low-dose vaginal estrogen cream have demonstrated efficacy for reducing symptoms of atrophic vaginitis. Dr. Bachmann reported findings from a randomized clinical trial comparing the two regimens.

Both active-therapy regimens led to significantly greater improvement in all outcome measures at 12 weeks compared with placebo.

A total of 155 patients treated with either regimen of vaginal estrogen cream had evaluable endometrial biopsies. In the patients assigned to daily therapy, six of 85 had evidence of proliferative endometrium. Among 72 assigned to twice-weekly treatment, six had proliferative endometrium.

In general, adverse events were similar in the active-treatment and placebo groups, Dr. Bachmann reported, and treatment-emergent adverse events were uncommon. Treatment-emergent vaginal bleeding occurred in no more than two patients in any randomized group during the double-blind and open-label phases of the study.

MedPage Today

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September 15, 2008 — Sticking with any diet is difficult, but the incentives of adhering to the traditional Mediterranean diet are particularly beneficial, a new meta-analysis has shown [1]. Strictly following the Mediterranean diet reduced the risk of dying from cancer and cardiovascular disease as well as the risk of developing Parkinson's and Alzheimer's disease, and investigators say that greater adherence can be a relatively simple tool to reduce the risk of premature death in the general population.

"The practical implication is that we are able to talk to our patients and show them that sticking to this diet, the specific characteristics of the diet, improves their overall health and quality of life," lead investigator Dr Francesco Sofi (University of Florence, Italy) told heartwire. "This is good information to give, especially if we're able to tell them something as simple as eating more fruits and vegetables."

The meta-analysis, published online September 12, 2008 in BMJ, included primary-prevention studies that assessed how well individuals stuck to the traditional Mediterranean diet and whether this translated into health benefits. In each of the 12 trials included in the meta-analysis, which included more than 1.5 million patients followed from three to 18 years, a numerical score, known as the adherence score, was used to assess how closely individuals were following the diet. A score of zero indicated low adherence to the diet, while a score of 7 to 9 points indicated high adherence to the Mediterranean diet.

Individuals who stuck strictly to a Mediterranean diet—defined as a two-point increase in the adherence score—had significant improvements in their overall health, including a 9% reduction in all-cause mortality, a 9% reduction in mortality from cardiovascular disease, and 6% reduction in cancer mortality. Although only three trials examined the association between adhering to the diet and the risk of Parkinson's and Alzheimer's disease, there was a reduced risk of these diseases when individuals closely followed the Mediterranean diet.

"The results overall showed that increasing two points on the adherence score results in a significant protective effect in terms of chronic diseases," said Sofi. "The study supports the current guidelines and recommendations of all the current scientific organizations that encourage the Mediterranean diet. It does say more, however, in terms of adherence, meaning it is important to actually stick with the diet."

In terms of applying the findings to the real world, Sofi said creating an adherence score based on "a theoretically defined Mediterranean diet" could be used as preventive tool for reducing the risk of mortality and morbidity in the general population. However, he added, it is important to define the diet properly.

"The problem with the literature is that a lot of papers suggest eating in a Mediterranean way, but what is the Mediterranean way? That's the problem. If you ask two subjects, you're going to get two different answers. We need to attempt to develop the characteristics of the Mediterranean diet and create the adherence score based on that."

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OSLO, Sept. 19 -- Thinner men in middle age, or those who lose substantial weight as they grow older, may have brittle bones in their 70s, researchers here said.

Some 15.1% of men who lost 10% or more of their body weight after their late 40s had osteoporosis when they reached 75, compared with 0.6% of those who had weight gains of at least 10%, reported Haakon E. Meyer, M.D., Ph.D., of the University of Oslo, and colleagues in the Aug. 15 issue of the American Journal of Epidemiology.

The researchers, who studied nearly 1,500 men over a 30-year period, found that combination of low initial weight and subsequent weight loss was an even stronger risk factor for osteoporosis.

"Low BMI in middle-age men was related to the risk of osteoporosis three decades later and ... this risk was modulated considerably by later weight change," Dr. Meyer and colleagues wrote. They said a clinical implication of their findings is that weight loss, while generally beneficial, is not risk-free. "When considering weight-loss interventions, the effect on osteoporosis and fracture should also be included and, if possible, counteracted," they suggested.

Slimness and short-term weight loss are already recognized as a risk factor for osteoporosis for men as well as women, the researchers said, but their effects had not previously been studied for such a long period.

The new findings emerged from studies of 1,476 Norwegian men in the cities of Oslo and Tromsø who underwent general health exams from 1972 to 1975 and again from 2000 to 2001. The follow-up screening also included bone mineral density testing of the hip.

They also estimated that men in the lowest quartile of BMI who lost at least 5% of body weight would be 2.79 times as likely to suffer a future hip fracture relative to those in the highest quartile and with stable weight.

"Weight change might act on the skeleton through changes in mechanical loading, changes in mechanical muscle stress, changes in hormone regulation of bone metabolism, and changes in intake of nutrients," the researchers wrote in addressing possible mechanisms.

Altered smoking habits or physical activity can affect weight as well as osteoporosis risk, they said.

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September 15, 2008 — Sticking with any diet is difficult, but the incentives of adhering to the traditional Mediterranean diet are particularly beneficial, a new meta-analysis has shown [1]. Strictly following the Mediterranean diet reduced the risk of dying from cancer and cardiovascular disease as well as the risk of developing Parkinson's and Alzheimer's disease, and investigators say that greater adherence can be a relatively simple tool to reduce the risk of premature death in the general population.

"The practical implication is that we are able to talk to our patients and show them that sticking to this diet, the specific characteristics of the diet, improves their overall health and quality of life," lead investigator Dr Francesco Sofi (University of Florence, Italy) told heartwire. "This is good information to give, especially if we're able to tell them something as simple as eating more fruits and vegetables."

The meta-analysis, published online September 12, 2008 in BMJ, included primary-prevention studies that assessed how well individuals stuck to the traditional Mediterranean diet and whether this translated into health benefits. In each of the 12 trials included in the meta-analysis, which included more than 1.5 million patients followed from three to 18 years, a numerical score, known as the adherence score, was used to assess how closely individuals were following the diet. A score of zero indicated low adherence to the diet, while a score of 7 to 9 points indicated high adherence to the Mediterranean diet.

Individuals who stuck strictly to a Mediterranean diet—defined as a two-point increase in the adherence score—had significant improvements in their overall health, including a 9% reduction in all-cause mortality, a 9% reduction in mortality from cardiovascular disease, and 6% reduction in cancer mortality. Although only three trials examined the association between adhering to the diet and the risk of Parkinson's and Alzheimer's disease, there was a reduced risk of these diseases when individuals closely followed the Mediterranean diet.

"The results overall showed that increasing two points on the adherence score results in a significant protective effect in terms of chronic diseases," said Sofi. "The study supports the current guidelines and recommendations of all the current scientific organizations that encourage the Mediterranean diet. It does say more, however, in terms of adherence, meaning it is important to actually stick with the diet."

In terms of applying the findings to the real world, Sofi said creating an adherence score based on "a theoretically defined Mediterranean diet" could be used as preventive tool for reducing the risk of mortality and morbidity in the general population. However, he added, it is important to define the diet properly.

"The problem with the literature is that a lot of papers suggest eating in a Mediterranean way, but what is the Mediterranean way? That's the problem. If you ask two subjects, you're going to get two different answers. We need to attempt to develop the characteristics of the Mediterranean diet and create the adherence score based on that."

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Women over 70 who get five hours of sleep a night or less may be more likely to fall than those who sleep seven to eight hours, according to a new study.

After controlling for age, body mass, alcohol use, sleep medications and many other variables, they found that women who slept less than five hours a night were about 47 percent more likely to have fallen twice or more in the course of the study.

Analysis showed that while a variety of factors associated with poor sleep might increase the risk of falls — depression, balance or gait problems — these things explained some, but not all, of the relationship. The association with shorter nighttime sleep remained an independent risk factor.

“People think getting less sleep is just a normal aspect of aging,” said Katie L. Stone, the lead author and a scientist at the California Pacific Medical Center Research Institute. “But you should bring it to the attention of your physician. There are options available for treatment.”

The New York Times

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Objectives: To investigate the relationship between markers of vitamin B₁₂ status and brain volume loss per year over a 5-year period in an elderly population.

Conclusion: Low vitamin B₁₂ status should be further investigated as a modifiable cause of brain atrophy and of likely subsequent cognitive impairment in the elderly.

NEUROLOGY 2008;71:826-832

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August 29, 2008 — As people grow older, they experience a substantial acceleration in cognitive decline — even if they don't have dementia, a new study suggests.

"Based on previous studies, we expected to see an acceleration in the decline in cognitive abilities before death," lead author Valgeir Thorvaldsson, from the department of psychology at Göteborg University, in Sweden, told Medscape Neurology & Neurosurgery. "However, the onset of this acceleration was much earlier than we expected."

Mr. Thorvaldsson said this was especially the case for perceptual speed, where the average onset of terminal decline was almost 15 years before death.

"The findings imply that the brain changes that influence cognitive abilities in old age occur over a relatively long period of time," he noted.

Their findings were published online August 27 in Neurology.

Medscape Today

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September 3, 2008 — Omega-3 fatty-acid supplementation improves morbidity and mortality in symptomatic heart-failure patients, while statins failed to have any beneficial effect in the same group of patients, two new studies have shown [1,2]. The long-term administration of omega-3 fatty acids reduced all-cause mortality and admission to the hospital for cardiovascular (CV) reasons, while there was no effect on these end points with 10-mg rosuvastatin (Crestor, AstraZeneca)....

Medscape Today

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September 3, 2008 — Results of a randomized trial show no evidence that extended-release dipyridamole (Aggrenox, Boehringer Ingelheim), aspirin, or telmisartan (Micardis, Boehringer Ingelheim) have neuroprotective effects on either disability due to a recurrent stroke or cognitive decline over time.

The results of this third factorial analysis of the Prevention Regimen for Effectively Avoiding Second Strokes (PROFESS) trial are published online August 29 in Lancet Neurology. Results of the other 2 main analyses, 1 comparing aspirin plus extended-release dipyridamole with clopidogrel for the prevention of recurrent stroke and another comparing telmisartan vs placebo in these same patients, were published online August 27 in the New England Journal of Medicine.

"PROFESS is the largest trial so far to investigate in a prespecified manner whether treatment with antiplatelet drugs or angiotensin II receptor agonists (such as telmisartan) are neuroprotective in patients who have had a recurrent stroke," the researchers, with first author Hans-Christoph Diener, MD, from the University of Duisberg/Essen, in Essen, Germany, conclude. "The degree of functional impairment at 3 months poststroke was similar across treatment arms."

The findings from all 3 analyses were previously presented at the 17th European Stroke Conference in Nice and reported by Medscape Neurology & Neurosurgery at that time.

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September 4, 2008 — Results of a new study show that among high-risk patients with atrial fibrillation admitted to the hospital for a stroke, the vast majority were either not taking warfarin or were in subtherapeutic ranges at the onset of the stroke. In fact, only 10% of patients admitted with a first ischemic stroke were found to be receiving warfarin and were in a therapeutic range at the time of their stroke.

"These findings should encourage greater efforts to prescribe and monitor appropriate antithrombotic therapy to prevent stroke in individuals with atrial fibrillation," the researchers, with first author David J. Gladstone MD, PhD, from Sunnybrook Health Sciences Center and the Institute for Clinical Evaluative Sciences in Toronto, Ontario, Canada, conclude.

Their results were released in the August 28 Online First issue and will appear in the January 2009 issue of Stroke.

Medscape Today

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September 5, 2008 — Post hoc analysis of data from the Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial shows no significant difference in the reduction of nonfatal or fatal stroke with atorvastatin (Lipitor, Pfizer) treatment vs placebo after a first stroke or transient ischemic attack (TIA) between older and younger patients in that trial, although the benefit trended to be higher for the younger age group.

"We found that there was no statistical difference in the results for prevention of stroke or some of the other outcomes" on the basis of age, lead author Seemant Chaturvedi, MD, from Wayne State University, in Detroit, Michigan, told Medscape Neurology & Neurosurgery. In addition, older patients receiving atorvastatin had significantly fewer cardiac events, including major coronary events and revascularization, compared with placebo, he added.

"Our conclusion is that clinicians should more strongly consider using statins after a TIA or stroke even in an elderly population," Dr. Chaturvedi said.

The analysis, using data from the SPARCL trial, is published online September 3 in Neurology.

Medscape Today

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August 29, 2008 — Survivors of stroke with long-term mobility impairment may benefit from a treadmill exercise rehabilitation plan, a new study shows. Reporting in the August 28 Online First issue of the journal Stroke, researchers describe evidence of neuroplastic mechanisms that may improve functional outcomes.

Medscape Today

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September 4, 2008 — Results of a randomized trial in older adults with subjective memory impairment but without dementia show a "modest" but lasting improvement in cognitive function after a 6-month program of physical activity.

"To our knowledge, this trial is the first to demonstrate that exercise improves cognitive function in older adults with subjective and objective mild cognitive impairment," the researchers, led by Nicola T. Lautenschlager, MD, from the University of Melbourne and St. Vincent's Hospital, in Australia, conclude. "The benefits of physical activity were apparent after 6 months and persisted for at least another 12 months after the intervention had been discontinued."

Their results are interesting given the relatively modest increase in physical activity, amounting to about 142 extra minutes per week, or 20 minutes per day, they note.

The study is published in the September 3 issue of the Journal of the American Medical Association.

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The study was conducted from 2004 to 2007 in metropolitan Perth, Australia. MELBOURNE,

Australia, Sept. 2 -- A six-month program of physical activity provided modest improvement in cognition over 18 months for older individuals with subjective memory impairment, a study found.

As the world population ages, the number of older adults living with Alzheimer's disease is estimated to increase from the current 26.6 million to 106.2 million by 2050, Nicola T. Lautenschlager, M.D., of the University of Melbourne, and colleagues, wrote in the Sept. 3 issue of the Journal of the American Medical Association.

If illness onset could be delayed by 12 months, they said, 9.2 million fewer cases of Alzheimer's would occur worldwide, they said.

To test whether a physical-activity intervention might delay progression of prodromal symptoms to full-blown dementia, the researchers conducted a randomized controlled trial of 138 patients who did not meet criteria for dementia but who reported memory problems and had lower scores on the cognitive section of an Alzheimer's disease scale.

Patients (about 40% women, mean age about 68) were randomly assigned to a 24-week, home-based exercise program or to an education and usual-care group.

At 18-month follow-up, the exercisers showed a statistically significant though modest difference of 0.69 points on cognitive tests compared with the usual-care control group.

Participants in the exercise group were asked to perform at least 150 minutes of moderate-intensity physical activity per week in three 50-minute sessions each week.

The most frequently recommended and used activity was walking. However, participants could choose light strength training or other aerobic exercise.

Participants also received regular mailed newsletters to reinforce the key messages of the program. The intervention did not include home-based equipment.

Individuals in the usual care group received educational material about memory loss, stress management, healthful diet, alcohol consumption, and smoking, but not about physical activity. Participants in the physical activity group were offered the same educational materials.

Those in the exercise group achieved 142 minutes more physical activity a week or 20 minutes a day more than those in the usual care group.

Cognitive function over 18 months was assessed with the Alzheimer Disease Assessment Scale -- Cognitive Substance Subscale (ADAS-COG), a measure that included 11 brief cognitive tests (possible range, 0 to 70).

In an intent-to-treat analysis, participants in the intervention group improved 0.26 points (95% confidence interval −0.89 to 0.54), whereas those in the usual-care group deteriorated 1.04 points (95% CI 0.32 to 1.82) on the ADAS-Cog measure.

At 18 months, participants in the intervention group improved 0.73 points (95% CI −1.27 to 0.03) on the ADAS-Cog, while those in the usual-care group improved only 0.04 points (95% CI −0.46 to 0.88) for a 0.69 difference.

Delayed word recall and Clinical Dementia Rating improved modestly as well, whereas total immediate word recall, digit symbol coding, verbal fluency, Beck depression score, and the Medical Outcomes summary did not change significantly.

Although the average improvement was small, it is potentially important given the relatively modest amounts of physical exercise undertaken by study participants, the investigators said.

The mechanisms by which physical activity improves cognition in these patients are not clear, the researchers said, but possible explanations include alteration in cerebral vascular function and brain perfusion or environmental enrichment associated with greater activity.

It is also possible that the benefits in this trial were attenuated by preexisting or ongoing deleterious effects of APOE ε 4, the researchers said.

Limitations of the study included the fact that the sample was relatively small and may not have represented the population at high risk for cognitive decline.

In addition, it was a single-site study, and the investigators had no access to brain imaging or biochemistry, making it impossible to study potential physiological mechanisms.

Finally, the researchers said, the study cannot be used to infer that physical activity reduces the risk of dementia among older adults, because it was not powered to investigate development of dementia.

But, the researchers said, physical activity has health benefits that are not confined to cognitive function alone as suggested by other findings for depression, quality of life, falls, cardiovascular function, and disability, the investigators said.

In an accompanying editorial, Eric B. Larson, M.D., of the Group Heath Center for Health Studies in Seattle, wrote that despite the statistically significant mean "improvement" in the exercise group of 0.74 versus 0.04 for the controls, neither patients, family members, nor clinicians could easily detect that level of difference.

On the other hand, Dr. Larson said, although it is easier to take a pill, patients and their families are likely to be gratified by the benefits of habitual exercise and often may be disappointed with the effects of cholinesterase inhibitors.

Neither exercise nor drugs are very potent and no evidence to date shows that either method can prevent conversion to Alzheimer disease, Dr. Larson said.

For an illness that starts so late in life, prevention means delaying onset, he said. If exercise is protective in delaying loss of cognition and if its effects can be sustained, presumably with minimum cost and adverse effects, then it is an attractive strategy in an increasingly aging society.

Future larger multi-site trials including persons older than 70 could test the effect of habitual exercise on cognitive decline and conversion to dementias. These studies could also evaluate which methods are most worthwhile in promoting behavior change, Dr. Larson concluded.

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The flip side of a longer life expectancy might be a much greater public health burden in caring for the very old and extremely disabled. But that is not the case, according to a new report.

The study, published online in the Proceedings of the National Academy of Sciences, tracked all Danes born in 1905 for seven years beginning in 1998. Most had died by the end of the study, but as the researchers examined them with four assessments at ages 94, 96, 98 and 100, the percentage living independently decreased only slightly in the seven-year span, to 32.7 percent from 38.9 percent.

At the same time, the small number of people who survived to age 100 — 156 of the original 2,234 — showed a significant increase in disability, to 67.3 percent at 100 from 30.1 percent at 92. The explanation for the apparent paradox, the authors write, is the high level of mortality among dependent participants. The few who survived the longest were least likely to be dependent at the start of the study.

“Some worry that extreme old age leads to extreme levels of disability,” said Dr. Kaare Christensen, the lead author of the study and a professor of epidemiology at the University of Southern Denmark. “But our study shows that people are no more dependent at 100 than at 92.”

The New York Times
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The aging of the population means a big increase in the number of people who have developed and will develop cataracts -- and a consequent increase in the demands on the ophthalmic surgeon. Moreover, the success of refractive surgery has created an awareness of and expectation for spectacle independence following cataract surgery. No longer simply satisfied with a return to unobstructed vision, cataract patients are increasingly demanding near 20/20 vision, as well as expecting good distance vision -- all without using spectacles or contact lenses.

In addition to these needs, the evolving technology and work and cultural needs of the 21st century have changed the paradigm of what outcomes are most desired from lens replacement surgery. One change in particular is the new-found importance of "intermediate vision." As computers, personal device assistants (PDAs), and other handheld or arms-length technologies become more prominent for work and social networking, I have increasingly seen patients requesting intermediate vision at the expense of near vision. This preference represents a stark transition from a prioritization of near, low-field vision -- such as that that results from bifocals -- that sufficed when books and printed material dominated our near experience.

Concurrent to changing patient demands is an increased repertoire of tools available to the cataract surgeon. Although a select field of ophthalmologists had been working with the refractive mentality and skill set for 10 years or more, it was the medical industry itself that created new intraocular lens (IOL) designs that created the push toward spectacle-free independent cataract surgery......

However, at the heart of the transition to spectacle independence is the development of a new generation of IOLs. What follows is a discussion of the currently available IOLs, along with some of their benefits and drawbacks, based on the available research and on the author's clinical experience.

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SANTA MONICA, Calif., Aug. 22 -- Older smokers doubled their quit rate when given nicotine patches and access to telephone counseling, showed a Medicare demonstration program.

The one-year quit rate was almost 20% compared with 10% for smokers who received a brochure about smoking cessation (usual care), Geoffrey Joyce, Ph.D., of the RAND Corp. here, and colleagues, reported online in Health Services Research.

Physician counseling and the combination of counseling and medical therapy also led to higher quit rates compared with usual care.

"The results of this study suggest that a fully integrated [Medicare] benefit structured around low-cost pharmacotherapy in conjunction with available free quitline services would substantially reduce the prevalence of smoking and smoking-related illness among elderly beneficiaries motivated to quit, at a relatively modest cost," the authors concluded.

Smoking-cessation efforts have primarily targeted the young, before they become habitual smokers. However, increasing evidence suggests that quitting smoking after decades of exposure can substantially reduce smoking-related illness, the authors noted.

"A person smoking twenty or more cigarettes per day and who quit at age 65 could expect to increase their life expectancy by two to three years, in addition to any improvements in quality of life," they said.

Most private and public health plans do not fully cover smoking-cessation services, in part because of a lack of evidence that insurance coverage increases long-term abstinence, particularly among older adults who often have smoked for decades.

Medicare beneficiaries in the seven states were recruited into four intervention groups:

A brochure about smoking cessation (usual care).
Reimbursement for four counseling sessions with a physician.
Reimbursement for counseling and smoking-cessation drug therapy (nicotine patches or bupropion [Zyban]).
Nicotine patches plus a telephone hotline.

The six-month quit rates were 9.9% with usual care, 11.9% with provider counseling, 15.8% with counseling plus drug therapy (P=0.05 versus usual care), and 21.2% with nicotine patches plus telephone counseling (P=0.05 versus usual care). At 12 months, the quit rate with usual care (10.2%) was significantly lower compared with each of the other interventions (P=0.05):

14.1% with provider counseling
15.8% with counseling plus drug therapy
19.3% with nicotine patches plus telephone counseling and support

"Rates of confirmed smoking cessation in the Medicare Stop Smoking Program compared favorably with quit rates in the general population and were higher than expected for older adults," the authors said.

The authors noted several limitations of the study: imbalances in patient enrollment, lack of information about the number and quality of counseling sessions that participants in those groups received, and reliance on self-reported information and cessation rates.

MedPage Today
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AMSTERDAM, June 10 -- For older patients who have dementia, bright lighting may help correct circadian rhythms and improve cognitive and physical functioning, researchers found.

Compared with patients in assisted living facilities who were exposed to lower levels of light in the dayroom, those exposed to bright lighting had less cognitive deterioration, fewer depressive symptoms, and a slower decline in functional limitations, Eus Van Someren, Ph.D., of the Netherlands Institute for Neuroscience here, and colleagues reported in the June 11 issue of the Journal of the American Medical Association.

A daily dose of melatonin had mixed effects, they said, improving sleep quality but worsening mood and increasing withdrawn behavior.

Therefore, the researchers said, melatonin's "long-term use by elderly individuals can only be recommended in combination with light to suppress adverse effects on mood."

In older patients with dementia, cognitive decline is frequently accompanied by changes in mood, behavior, sleep, and activities in daily living, which may be influenced by changes in the circadian pacemaker in the brain, the researchers said.

The mean duration of the study was 15 months (maximum 3.5 years).

Bright lighting alone was associated with a relative 5% attenuation of cognitive decline, as measured on the Mini-Mental State Examination (P=0.04).

Bright lights also reduced depressive symptoms by a relative 19% (P=0.02), slowed the increase in functional limitations by a relative 53% (P=0.003), and increased total sleep duration by 2% (P=0.04).

Treatment with melatonin alone shortened sleep onset latency by 19% (P=0.02), increased sleep duration by 6% (P=0.004), and lengthened the average duration of uninterrupted periods of sleep by 25% (P=0.02).

However, the hormone was associated with worse scores on the positive scale of a mood assessment (P=0.02) and higher scores on the negative scale (P=0.01), as well as an increase in withdrawn behavior (P=0.02).

All three of these negative effects were diminished when melatonin was combined with exposure to bright lights, the researchers said.

The combined treatment also reduced agitated behavior by 9%, increased sleep efficiency by 3.5%, improved nocturnal restlessness by 9%, and reduced the average duration of individual awakenings at night by 12% (P=0.01 for all).

None of the treatments increased the occurrence of adverse events and the bright lights reduced dizziness, headache, inability to sleep, irritability, and constipation, which was also reduced by melatonin.

In terms of whether the effects were clinically significant, the researchers concluded, "On the whole, light treatment could have clinically beneficial effects."

For instance, they said, the combined effects of melatonin and bright light on sleep, if sustained over time, "could help maintain sleep efficiency above 85%, which has been regarded as a cutoff for clinically relevant disturbed sleep."

Also, interpretation of the results should be done with caution, they said, because of the multiplicity of analyses and outcomes in the study.

Primary source: Journal of the American Medical Association

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The baby boom generation is 78 million adults who begin to turn 65 in 2011. Unless we make changes now, we will not have enough doctors, nurses, and other caregivers prepared to meet the health needs of older Americans.

Too few doctors and nurses are choosing to specialize in geriatrics; less than 1% of all doctors are geriatricians. Informal caregivers -- that is, patients and their family members and friends -- are often ill-prepared to handle the necessary treatments and specialized care that elders require.

To ensure that older Americans receive appropriate and high-quality care, the Institute of Medicine recommends the following steps in its report Retooling for an Aging America: Building the Health Care Workforce:[1]

First, instead of relying predominantly on specialists, we should work to enhance the competence of all individuals involved in the delivery of geriatric care.

Second, at the same time, we need stronger incentives to recruit and retain geriatric specialists and caregivers.

Finally, we need to apply more flexible models of care so that patients and those with lesser amounts of training can do more. For example, new home-based technologies offer an exciting prospect of enabling self-care by patients and other informal caregivers.

By retooling the health workforce, we can help assure that every American can look forward to a healthier future.

That's my opinion. I'm Dr. Harvey Fineberg, President of the Institute of Medicine.

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Despite her racing pulse and falling blood pressure, the 81-year-old patient was still alert. She was also terrified. Earlier that day, she said in a quavering voice, her leg had started to throb. Then the throb became a bruise. Now, her leg was swollen, cool — and lifeless.

As I gently touched her thigh, I felt the crackle and pop of tiny pockets of air beneath her skin. I looked up and found the woman’s eyes searching mine. Am I dying? they seemed to ask.

I gave her hand a little squeeze. “The antibiotics are already at work,” I told her, as calmly as I could.

Then I returned to the banshees in my brain. “Do this! Do that!” they screeched. The case was an all-out emergency. The moment for intimate conversation with the patient had passed.

Of all the mayhem an infectious-diseases doctor sees in a lifetime, nothing tops spontaneous gas gangrene. One day, out of the blue, a human body part is invaded by large, snub-nosed bacteria from the gut. Once planted in foreign flesh, the organisms — Clostridium perfringens — ferment gas, spew toxins and mutilate muscle. Soon, blisters erupt, and after that point few victims survive. Even with aggressive surgery and industrial-strength antibiotics, their odds are poor.

But this is not so much a story about a rare, violent ambush by a micro-organism as about a doctor and a patient, staring death in the face. That’s what the 81-year-old woman was doing, and from countless wordless clues — her wide-eyed gaze, the periodic flutter of her hand to a cross around her neck — I believe she knew it. These days, when death’s footfalls are often silenced by drugs and machines, not many people have the chance to confront their fate so squarely.

Of course we all expect to go — sometime. As the economist John Maynard Keynes memorably put it, “In the long run, we are all dead.” But Keynes wrote those cool words decades before his own death. Who among his tribe — or the current tribe of medical professionals, for that matter — wants to pull the plug on hope at that moment?

Call me weak, but when I was trying to care for the dying woman, I didn’t.
Were things different in the old days? I’m now well into my 50s. Several of my early mentors began their careers before the era of antibiotics. Back then, although the weapons at their disposal were meager, they took more time to talk. They also understood that some deadly diseases were accompanied by a brief window of crystalline awareness. On that list, curiously enough, was clostridial myonecrosis, or gas gangrene — the same wildfire that consumed my patient’s leg.

Observing her inspired me to note the mental and emotional clarity of other patients under sudden, desperate microbial siege. Sure enough, not much later, I met a recently divorced middle-age man who was uncommonly lucid in the face of disaster. Having just returned from an African safari, he arrived at our emergency room with a fever of 105 and a sleeping-sickness infection so dense that two or three sinuous organisms could be seen in every microscopic field of his blood. Simply put, a biologic tinderbox. The only good thing was that his rapidly multiplying parasites had not yet breached his brain.

Now picture a university emergency room circa 1990, minus cellphones. So certain was my patient that he was about to die — and so aware of the implications of his death — that the critically ill man refused all care until a nurse wheeled him to a desk. Why? He wanted to call his lawyer and change his will.

Fortunately, his story ended well. Although his infection and its toxic cure caused multiple organ failure, he recovered and three weeks later was able to leave the hospital. Today he is happily remarried. From time to time, we still talk about his whisper-close brush with death.

Sadly, there was no next chapter for the lady with gas gangrene. An hour after I met her, she was unresponsive. A few hours later, with her family at her side, she died. She never made it to the operating room, and as far as I know, none of her doctors discussed her imminent death, then simply sat with her.

Of course one could argue that there was no time, there was no need, she already knew, why add to her pain? But looking back, I still wish I had.

The New York Times

BALTIMORE, Aug. 18 -- Patients 65 and older are less likely to be transported to a trauma center than those who are younger, a retrospective database study showed.

Only half of all older trauma patients were taken to one of eight state-designated trauma centers, compared with more than 80% of younger patients (P<0.001), David Chang, Ph.D., M.P.H., of Johns Hopkins, and colleagues, reported in the August issue of Archives of Surgery.

Emergency medical services and trauma center personnel ranked the top three potential reasons for the undertriage as inadequate training on how to handle older trauma patients, a lack of familiarity with protocol, and possible age bias.

"The problem of age bias raised in this study may negate efforts to improve clinical care for elderly trauma patients within trauma centers if the system as a whole does not function properly and deliver patients appropriately to needed resources," the researchers said.

Although guidelines recommend treating older patients as aggressively as younger patients, some studies have found that age bias remains an issue in trauma care, they said.

To determine whether age bias played a role in determining which patients were taken to a trauma center, the researchers analyzed data from a 10-year period on 26,565 trauma patients from the Maryland Ambulance Information System.

Patients were included in the study if they met criteria for trauma defined by the American College of Surgeons, which included information on presenting physiology, injury pattern, and mechanism of injury, and were classified as priority I status -- critically ill or injured and requiring immediate attention -- by EMS personnel.

The undertriage rates were higher among patients 65 and older in all subgroups, including patients who expressed a preference for a specific hospital (70.8% versus 29.7%) and those who were taken to the closest hospital (68.1% versus 36.8%) (P<0.001>

In a multivariate analysis, patients 65 and older were 52% less likely to be transported to trauma center than younger patients (OR 0.48, 95% CI 0.30 to 0.76).

All patients ages 50 and older had a significantly lower likelihood of being taken to a trauma center than younger patients. Those 50 to 69 were 33% less likely to be taken to a trauma center (OR 0.67, 95% CI 0.57 to 0.77) and those 70 and older were 55% less likely (OR 0.45, 95% CI 0.39 to 0.53).

The researchers presented the findings to EMS and trauma center personnel and then surveyed 166 of them about possible reasons for the differences.

They were asked to provide a percent weight to the various possible reasons that could have contributed to the disparity. The top three were as follows:

• Inadequate training in handling older trauma patients (25.3%)
• Transport to a trauma center not worth it because of age, which the researchers defined as age bias (13.4%)
• Unfamiliarity with triage protocol (12%)

"Survey results suggest that lack of training related to elderly trauma patients and unfamiliarity with protocol may be allowing unconscious bias to affect triage decisions and that this problem occurs among both EMS providers and medical personnel at the receiving trauma centers," the researchers said.

They suggested retraining providers with triage protocols and highlighting literature that shows that older trauma patients can return to productive lives after an injury.

In an invited critique, Richard Mullins, M.D., of Oregon Health & Science University in Portland, wrote that "the authors dismissed three pertinent issues."

First, he noted that there is no evidence that older trauma patients would benefit from treatment at a trauma center.

Second, he said, only 20% of Maryland's hospitals are designated trauma centers, and trauma systems improved survival only in states with at least half of their hospitals designated as trauma centers. "Elderly patients are undertriaged in Maryland because rural hospitals are excluded from the state's trauma system," he said.

Finally, Dr. Mullins noted, mandatory admission to a trauma center may go against an older patient's wishes in regard to end-of-life decisions.

"Trauma surgeons must advocate for the inclusion of seriously injured elderly patients in statewide trauma systems but should also recognize that optimal care may be determined by the elderly patient's unique priorities and preferences," he concluded.

MedPage Today

PALO ALTO, Calif., Aug. 11 -- Regular running in middle age and beyond may lengthen lifespans and retard the disabilities of aging, a longitudinal study showed.

Runners ages 50 to 72 had a 40% reduced risk of being moderately disabled or of dying after a 21-year follow-up than healthy controls, Eliza Chakravarty, M.D., of Stanford, and colleagues reported in the Aug. 11 issue of the Archives of Internal Medicine.

Disability and survival curves continued to diverge between groups after the 21-year follow-up as participants approached their ninth decade of life, they added.

"Our findings of decreased disability in addition to prolonged survival among middle-age and older adults participating in routine physical activities further support recommendations to encourage moderate to vigorous physical activity at all ages," the researchers said.

The study began in 1984, when 538 members of a nationwide running club for those 50 and older and 423 healthy controls -- Stanford faculty and staff members ages 26 to 70 -- were recruited to complete yearly questionnaires.

At baseline, runners were younger (mean age 58 versus 62), leaner, more likely to be male, and less likely to smoke than the controls (P<0.001>

Both groups had little disability -- measured using the Health Assessment Questionnaire Disability Index (HAQ-DI), which asked the participants about their level of difficulty in completing eight tasks -- but runners had a significantly lower mean score compared with controls (P<0.001).>

Two previous reports on this cohort showed that disability was decreased and survival was increased in runners at eight and 13 years of follow-up.

A total of 284 runners and 156 controls completed the study through 21 years of follow-up, and the results extended the previous findings.

Disability scores increased with time for both groups, but at a significantly greater rate for the controls (0.016 points/year versus 0.007, P<0.001).>

Runners took longer to reach various levels of disability compared with controls -- for example, it took 2.6 years for controls to reach a mean HAQ-DI score of 0.075 and 8.7 years for runners, for a difference of 6.2 years (95% CI 3.9 to 8.9).

Among participants who had a baseline disability score of zero, runners had a significantly lower risk of being moderately disabled (HR 0.62, 95% CI 0.46 to 0.84).

Through follow-up, 15% of runners died compared with 34% of controls (P<0.001).>

Rates of death were higher in controls than in runners for cardiovascular disease (P=0.001), cancer (P=0.004), neurological disease (P=0.007), infections (P<0.001),>

The study's findings were similar when the participants were divided into ever-runners -- those who ran regularly for more than one month at some point in their lives -- and never-runners.

The authors suggested several possible reasons for the disability and survival advantages found in runners, including "increased cardiovascular fitness and improved aerobic capacity and organ reserve, increases in skeletal mass and metabolic adaptations of muscle with decreased frailty, lower levels of circulating inflammatory markers, improved response to vaccinations, and improved higher-order cognitive functions."

They acknowledged some limitations, including the self-reported data, possible self-selection bias, and potential confounding by unmeasured lifestyle variables.

In addition, they said, the results of the study may not be generalizable beyond the mostly white and college-educated study population.

DAVIS, Calif., July 29 -- For patients with knee osteoarthritis, an extract of the Indian frankincense plant gave significant pain relief and reduced levels of a marker of joint pathology, researchers here said.

Patients in a randomized, double-blind, 90-day trial showed significantly greater reductions in pain scores with the agent than with placebo, reported Siba R. Raychaudhuri, M.D., of the University of California Davis, and colleagues online in Arthritis Research and Therapy.

Synovial fluid levels of matrix metalloproteinase-3 also declined significantly in patients receiving the agent, whereas MMP-3 levels rose in the placebo group.

This was the agent's first randomized, placebo-controlled trial in osteoarthritis of the knee, the researchers said.

The agent, tradenamed 5-Loxin, was derived from Boswellia serrata, a plant that has long been prominent in the Ayurvedic system of traditional Indian medicine. It is already widely marketed in the U.S. as a nutritional supplement, with purported benefits including enhanced joint mobility and function.

The extract contains 30% 3-O-acetyl-11-keto-beta-boswellic acid, identified in laboratory and animal studies as the anti-inflammatory component, according to Dr. Raychaudhuri and colleagues.

In particular, the compound appears to inhibit 5-lipoxygenase, a key intermediate in the inflammatory cascade.

The study assigned 70 patients to placebo or to 100 mg or 250 mg of the extract, given orally in divided doses.

Patients at baseline had mean pain scores, on a visual analogue scale, of 56 to 57 points.

At the end of treatment, mean scores in the placebo group were 41.8 (SD 16.0), compared with 21.4 (SD 7.1) in the low-dose treatment group and 14.2 (SD 6.8) for those in the high-dose group. The declines in both treatment groups were significantly greater than in the placebo group (P<0.0001).

Similar results were also seen in the pain subscale of the Western Ontario and McMaster Universities Osteoarthritis Index (WOMUOI).

Improvements in pain scores with the agent were noted in one week in some patients, the researchers aid.

Functional assessments, including the WOMUOI stiffness and functional subscales and Lequesne's Functional Index, also showed significant advantages for the plant extract versus placebo.

For example, mean stiffness scores in the placebo group declined from 33.2 (SD 2.7) at baseline to 24.5 (SD 2.4) after treatment, whereas in the low-dose treatment group, mean scores fell from 31.8 (SD 3.6) at baseline to 14.1 (SD 3.7) following treatment (P<0.0001 versus placebo).

As with the pain scores, greater improvements were seen in the high-dose group: stiffness scores decreased from 27.8 (SD 3.4) at baseline to 9.24 (SD 2.1) after treatment (P<0.0001).

Mean MMP-3 levels in synovial fluid increased slightly in the placebo group, from 902.1 ng/ml (SD 275.1) at baseline to 928.5 (SD 216.0) following treatment.

In the low-dose and high-dose treatment groups, MMP-3 levels fell substantially: from 893.6 (SD 270.1) and 926.9 ng/ml (SD 270.5) at baseline, respectively, to 637.2 (SD 224.5) and 497.5 (SD 167.5) ng/ml after treatment (both P<0.0001 versus placebo).

MMP-3 is a cartilage-degrading enzyme. Its presence in synovial fluid is a marker of joint destruction.

"5-Loxin has potential efficacy in terms of reducing pain and improving the physical ability of osteoarthritis patients," Dr. Raychaudhuri and colleagues wrote.

In combination with animal experiments that found no mutagenic effects or other major toxicity concerns, the adverse event profile in the clinical trial indicates that the compound "is potentially safe in the treatment of osteoarthritis in humans," the researchers said.

Dr. Raychaudhuri and colleagues said the most common adverse effects were diarrhea, nausea, abdominal pain, mild fever, and general weakness, without significant difference between placebo and the active treatment groups.

CHICAGO, July 29 -- The rate of new cases of mild cognitive impairment in patients over 70 is higher than previously expected, results from the Mayo Clinic Study of Aging showed.

Initially healthy participants developed mild cognitive impairment at a rate of 5.3% a year (95% CI 4.3% to 6.5%), two to three times higher than the rate of new cases of dementia in the same population, Ronald Petersen, M.D., Ph.D., of the Mayo Clinic in Rochester, Minn., reported at the International Conference on Alzheimer's Disease here.

"If we extrapolate Alzheimer's incidence rates to mild cognitive impairment, we would expect perhaps 1% to 2% per year," said Dr. Petersen, who is also the vice chair of the Alzheimer's Association's medical and scientific advisory council, "but our findings were substantially higher than that."

The rate increased from 3.5% (95% CI 2.4% to 5%) in participants ages 70 to 79 to 7.2% (95% CI 5.5% to 9.3%) in those ages 80 to 89.

In addition, men were nearly twice as likely as women to develop mild cognitive impairment (HR 1.92, 95% CI 1.22 to 3.02).

Although mild cognitive impairment may represent a transitional phase to various forms of dementia, it is unknown how often it occurs in a population-based setting, the researchers said.

To find out, they turned to the Mayo Clinic Study on Aging, which randomly selected participants ages 70 to 89 from Olmsted County, Minn., in 2004; 1,786 participants were available for analysis.

Each participant underwent a baseline examination that included an assessment of cognitive function and a neurological exam. In addition, the researchers interviewed a close acquaintance of each participant. Follow-up was conducted in 15-month intervals.

The rates of mild cognitive impairment in men and women were 6.2% (95% CI 4.7% to 8.1%) and 4.4% (95% CI 3.1% to 6%), respectively.

Compared with women, men were more likely to have amnestic mild cognitive impairment (HR 2.00, 95% CI 1.12 to 3.57) as well as the non-amnestic subtype (HR 1.82, 95% CI 0.87 to 3.81), although the latter comparison did not reach statistical significance.

"These results underscore the urgency of developing new and better strategies to create disease-modifying therapies for Alzheimer's," Dr. Petersen said. "In addition, for public health purposes, we need to know how many people are cognitively impaired and potentially on the road to Alzheimer's."

Ralph Nixon, M.D., Ph.D., of New York University, and a member of the medical and scientific advisory council of the Alzheimer's Association, said, "This both magnifies the urgency of the problem of Alzheimer's disease and extends it to an even larger population but also gives some hope of early intervention that would target this population at an earlier stage of the disease."

According to Dr. Petersen, the findings may not be generalizable to populations outside of the predominantly white population of northern European descent of Olmsted County.

He noted, however, that the results of worldwide studies of mild cognitive impairment were not "drastically" different from those of the current study.

The findings are particularly important considering the shifting population distribution associated with aging baby boomers, Dr. Petersen said.

CHICAGO, July 29 -- Diabetics who took both insulin and other medications for the disease had fewer plaques associated with Alzheimer's disease than other patients, researchers said here.

In a postmortem study, patients on combination treatment had significantly fewer beta-amyloid plaques (P=0.014) than diabetics who were on one treatment alone or patients who did not have diabetes, Michal Schnaider Beeri, Ph.D., of Mount Sinai School of Medicine in New York, reported at the International Conference on Alzheimer's Disease.

Overall, the combination group had about 80% fewer plaques compared with the other groups combined.

However, there were no significant between-group differences in the occurrence of neurofibrillary tangles.

"These results suggest that the combination [of insulin and other diabetes medications] … may beneficially influence Alzheimer's-related brain changes," Dr. Beeri said. "This also points to biological pathways in the brain, such as insulin signaling, that might be a focus for developing new treatment strategies."

Because diabetes has been associated with a greater risk of mild cognitive impairment and Alzheimer's disease in epidemiological studies, the researchers expected to see more plaques when they examined the brains of diabetics.

In a previous study by Dr. Beeri's group, however, that wasn't the case. In fact, they found fewer plaques. Other neuropathological studies have failed to find any association between diabetes and the number of plaques or neurofibrillary tangles.

Dr. Beeri and her colleagues hypothesized that the treatments for diabetes may influence the neuropathology of Alzheimer's.

To test the hypothesis, the researchers studied 248 brains -- 124 from diabetics and 124 from non-diabetics -- from the Mount Sinai School of Medicine Brain Bank. Most of the specimens came from the Jewish Home and Hospital in Bronx, N.Y., and the two groups were matched by age, sex, and severity of dementia.

The mean age of the patients at death was 81.2 and 57.3% were female. The mean clinical dementia rating was 2.4, indicating moderate to severe dementia.

Non-diabetics had slightly lower body mass indices but the difference was not statistically significant.

Of the diabetics, 29 were not on any medication, 49 were taking insulin only, 28 were taking medications other than insulin -- like glyburide or metformin -- and 18 were taking both insulin and another diabetes medication.

The researchers examined the extent of plaques and neurofibrillary tangles in several neocortical regions and in the hippocampus, entorhinal cortex, and amygdala using the CERAD (Consortium to Establish A Registry for Alzheimer's Disease) neuropathological battery.

The group that was on combination treatment for diabetes had significantly fewer beta-amyloid plaques in the entorhinal cortex (P=0.003), amygdala (P=0.009), and overall (P=0.014) compared with the other groups, which did not differ significantly from each other.

The differences approached statistical significance in the hippocampus (P=0.057) and the combined neocortical measure (P=0.052).

When the researchers additionally controlled for APOE e4 genotype, BMI, and fasting glucose at the time of nursing home admission, there was no change in the findings.

Dr. Beeri acknowledged some limitations of the study, including the inability to determine causation and potential confounding. Nor could the survivor effect be ruled out, she said.

Nevertheless, Dr. Beeri said, the results suggest that diabetes medications may influence biological pathways involved in beta-amyloid processing.

Older patients who take statins may be at lower risk of developing dementia, according to findings from a prospective cohort study.


Statin users were 44% less likely to develop dementia and cognitive impairment than nonusers after controlling for other factors (P=0.010), reported Mary N. Haan, Dr.P.H., of the University of Michigan here, and colleagues in the July 29 issue of Neurology.

However, the findings were not enough to suggest that patients should take a statin unless necessary for other health reasons, the investigators cautioned.

Although these findings add evidence in favor of statins for cognitive outcomes, this area of research has been controversial with little agreement between studies, the researchers said.



At baseline, statin users and nonusers were similar, except that statin users were slightly younger, more educated, and more likely to have been born in the U.S. and covered by medical insurance.

Statin users were also more likely to have a history of diabetes and higher mean baseline cognitive scores on the Modified Mini-Mental State Examination.

During more than five years of follow-up, 130 participants developed dementia or cognitive impairment without dementia.

Of the 82 patients with dementia, 48% had possible or probable Alzheimer's disease, 23% had undetermined etiology, 13% had ischemic vascular dementia, and 13% had mixed Alzheimer's or vascular dementia.

Statin users had a 43% lower rate of dementia and non-dementia cognitive impairment than nonusers (hazard ratio 0.577, 95% confidence interval 0.376 to 0.886, P=0.012).

After controlling for baseline diabetes and stroke, statins remained associated with a 48% lower rate of dementia and non-dementia cognitive impairment (HR 0.518, 95% CI 0.336 to 0.797, P=0.003).

Further adjustment for education, smoking status, and apolipoprotein E (APOE-e4) genotype attenuated the association only slightly to a 44% lower risk compared with nonusers (HR 0.564, 95% CI 0.365 to 0.872, P=0.010).

The protective effect of statins on dementia held for both high functioning individuals with above-average cognitive scores on the Modified Mini-Mental State Examination (HR 0.546, 95% CI 0.327 to 0.912) and those with below average scores (HR 0.444, 95% CI 0.200 to 0.988).

The researchers cautioned that the findings may have been biased by differential loss to follow-up, indication bias, or competing risks.

However, they noted that statin use didn't appear to have an impact on survival (HR 0.92, 95% CI 0.69 to 1.20).


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Memory loss causes anxiety — which makes recall even harder. Here's a simple, inexpensive way to counter the problem by putting your "habit memory" to work. Memory loss is a fact of life for people with Alzheimer's disease. It's also quite common in people who've had traumatic brain injuries. Some of the memory training techniques used with brain-injured people are also proving helpful to people with mild cognitive impairment (MCI) — a disorder that often precedes Alzheimer's disease. Sherrie Hanna is the program coordinator of an ongoing study at Mayo Clinic in Rochester, Minn., to examine potential benefits of memory training for people who have MCI. In this interview, Hanna discusses the study's premise and its preliminary findings. What types of memory training techniques are you studying?

They say the 21st century is going to be the Asian Century, but, of course, it’s going to be the Bad Memory Century. Already, you go to dinner parties and the middle-aged high achievers talk more about how bad their memories are than about real estate. Already, the information acceleration syndrome means that more data is coursing through everybody’s brains, but less of it actually sticks. It’s become like a badge of a frenetic, stressful life — to have forgotten what you did last Saturday night, and through all of junior high.

In the era of an aging population, memory is the new sex.

[MORE]....The Great Forgetting - New York Times

Persistent Insomnia Blunts Response to Depression Treatment in Elderly...CLICK FOR FULL STORY

April 9, 2008 — Compared with their peers without insomnia, older patients with depression and persistent insomnia were up to 3.5 times more likely to have treatment-resistant depression, according to a recent study.

"We typically think of depression as a major disorder with symptoms such as insomnia, and that if we treat the depression, all these other bothersome symptoms will go away, but what this shows is that in some patients the insomnia doesn't go away," and the patients continue to be depressed, lead author Wilfred R. Pigeon, PhD, from the University of Rochester Medical Center, in Rochester, New York, told Medscape Psychiatry.

The clinical implications are that in the context of treating depression, "you should certainly ask about sleep and insomnia, and if insomnia is present, one should consider treating the insomnia at the same time as you treat the depression," he added.

The study is published in the April 1 issue of Sleep.


Cognitive Behavioral Therapy Shows Promise for Insomnia

"The findings from the current study do begin to build the case that persistent insomnia (as defined in this study) may blunt treatment response and serves as a barrier to remission from depression in a particular population and that this is especially true in older patients receiving standard primary care–based treatment of depression," the group summarizes.

"We now have data that shows that you can treat insomnia with cognitive behavioral therapy at the same time as you are treating depression with pharmacotherapy," Dr. Pigeon noted, adding that this was shown by Rachel Manber, PhD, at Stanford University, in Stanford, California, and colleagues, in a related article in the same issue of Sleep.

Medical News: Vigorous Walking May Slow Biological Aging to a Crawl - in Primary Care, Exercise & Fitness from MedPage Today

Vigorous Walking May Slow Biological Aging to a Crawl

Published: April 10, 2008

TORONTO, April 10 -- Vigorous walking for about an hour a day five times a week can chop a dozen years off the biological age of persons 64 and older, according to a researcher here.

A review of recent studies in patients age 64 and older showed that such a regimen can boost maximal oxygen intake by about 25% within three months, effectively decreasing biological age by about 12 years, Roy Shephard, M.D., Ph.D., of the University of Toronto, reported online in the British Journal of Sports Medicine.

This could also extend a patient's functional independence -- which is likely lost when maximal oxygen intake drops below 18 mL/kg/min for men and 15 mL/kg/min for women -- by about the same amount of time, he said.

The benefits of aerobic exercise increase the longer it is performed, he said.

"There remains a need to clarify the importance of deteriorations in fitness relative to other potential causes of dependency," he wrote, "but, from the practical viewpoint, regular aerobic activity can address many of the issues of both functional loss and chronic disease."

Past studies by Dr. Shephard suggested that keeping up aerobic fitness could stem the onset of dependency in older patients by maintaining functional capacity.

A program of endurance training could offset the expected loss of 5 mL/kg/min in maximal oxygen intake per decade, which equates to about 10 years of biological age, he said.

To assess the current state of knowledge on the subject, Dr. Shephard reviewed 30 studies published since 1990.

There was some uncertainty in the findings about the rate of decline of maximal oxygen intake in older patients.

The use of different study designs -- longitudinal or cross-sectional -- and the fact that most data were collected from relatively healthy participants made it difficult to compare the data.

"There is thus some inter-observer disagreement on the rate of deterioration during the retirement years," he wrote, "but is seems reasonable to postulate that a loss of at least 4 to 5 mL/kg/min per decade continues into advanced old age."

As maximal oxygen intake dropped through the years, the amount of activity a patient could participate in without becoming fatigued declined until functional independence was lost.

In one cross-sectional study, researchers found that the risk for dependency was increased by 14% for each 1 mL/kg/min loss in maximal oxygen intake in patients ages 55 to 86.

However, Dr. Shephard wrote, it remains difficult to determine how much of the risk of dependency comes from a reduction of aerobic fitness because, in most studies, few of the participants beginning a trial complete it, and those that do are generally more healthy.

The studies reviewed showed a trend toward greater gains in aerobic fitness with a longer training regimen. Average gains were 12.9% in an eight- to 10-week program, 14.1% in a 12- to 18-week program, and 16.9% with 24 to 52 weeks of training.

Those studies that used a high-intensity regimen reached the gains of 25%, which equals an increase in maximal oxygen intake of 6 mL/kg/min or a decrease of about 12 years of biological age.

Dr. Shephard noted that aerobic fitness may indirectly delay dependency by preventing other conditions that are likely to diminish functional capacity, including obesity, diabetes, hypertension, myocardial infarction, stroke, some forms of cancer, and osteoporosis.

Exercise also hastens recovery from injuries and any additional muscle power may prevent falls, he said.

"There seems good evidence that the conservation of maximal oxygen intake increases the likelihood that the healthy elderly person will retain functional independence," he said.

NEW YORK (Reuters Health) Feb 21 - Plasma levels of beta amyloid protein (A-beta) predict the risk of Alzheimer disease (AD) in elderly men, according to a report in the February issue of Archives of Neurology.

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Summary

The study enrolled 62 subjects taking 1 of 2 therapies for ocular hypertensive therapy: once-daily prostaglandin analog monotherapy or once-daily prostaglandin analog monotherapy plus a second ocular-hypotensive used once, twice, or three-times daily as prescribed. Adherence to monotherapy was good, and fewer than 10% of subjects had 5 or more dosing errors. However, the addition of a second drop resulted in much worse adherence and dosing errors of up to 37%. These findings occurred even though patients were not blinded to that fact that they were being monitored. No demographics affected the adherence rate, including age, gender, race, number of systemic medications, or severity of glaucoma..........CLICK HEADLINE FOR FULL STORY

Antidepressants: Selecting one that's right for you - MayoClinic.com

Daunted by the choice in antidepressants? With persistence, you and your doctor should find one that works so you can enjoy life more fully again. ( CLICK HERE TO VIEW FULL ARTICLE)

Physical Activity Linked to Lower Risk of Vascular Dementia But Not AD

Results of a new prospective study have found an association between increasing levels of physical activity and a lower risk for vascular dementia, but not for Alzheimer's disease (AD).

"Our findings show moderate physical activity such as walking and all physical activities combined lowered the risk of vascular dementia in the elderly, independent of several sociodemographic, genetic, and medical factors," first author Giovanni Ravaglia, MD, from University Hospital S. Orsola-Malpighi, in Bologna, Italy, said in a statement from the American Academy of Neurology. "It's important to note that an easy-to-perform moderate activity like walking provided the same cognitive benefits as other more demanding activities." (CLICK FOR FULL STORY)

CLICK:APA Releases Updated Guidelines for Dementia

CLICK FOR FULL STORYPlasma Beta Amyloid Predicts Alzheimer Disease Risk in Elderly Men

SAN DIEGO, April 8 -- Over-the-counter painkillers may promote muscle growth in older patients during weight training, a randomized, placebo-controlled study showed

In 24 patients with a mean age of 64, recommended daily doses of ibuprofen and acetaminophen were associated with gains of about 50% in muscle volume and strength compared with placebo after 12 weeks of resistance training, Chad Carroll, Ph.D., of Ball State University in Muncie, Ind., and colleagues reported at the Experimental Biology meeting here.

"These results suggest that chronic consumption of ibuprofen or acetaminophen during resistance training induces intramuscular changes that enhance the metabolic response to resistance exercise," said Todd Trappe, Ph.D., also of Ball State.

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Medical News: EB: OTC Painkillers Also Help Grandpa Get Buff - in Geriatrics, General Geriatrics from MedPage Today:

New York Times

NY Times Health

Causes »
Memory impairment is a necessary feature for the diagnosis of Alzheimer's or any type of dementia. Change in one of the following areas must also be present: language, decision-making ability, judgment, attention, and other areas of mental function and personality.

The rate of progression is different for each person. If AD develops rapidly, it is likely to continue to progress rapidly. If it has been slow to progress, it will likely continue on a slow course.

More than 4 million Americans currently have AD. The older you get, the greater your risk of developing AD, although it is not a part of normal aging. Family history is another common risk factor.
In addition to age and family history, risk factors for AD may include:
Longstanding high blood pressure
History of head trauma

High levels of homocysteine (a body chemical that contributes to chronic illnesses such as heart disease, depression, and possibly AD)

Female gender -- because women usually live longer than men, they are more likely to develop AD
There are two types of AD -- early onset and late onset. In early onset AD, symptoms first appear before age 60. Early onset AD is much less common, accounting for only 5-10% of cases. However, it tends to progress rapidly.

The cause of AD is not entirely known but is thought to include both genetic and environmental factors. A diagnosis of AD is made based on characteristic symptoms and by excluding other causes of dementia.
Prior theories regarding the accumulation of aluminum, lead, mercury, and other substances in the brain leading to AD have been disproved. The only way to know for certain that someone had AD is by microscopic examination of a sample of brain tissue after death.

The brain tissue shows "neurofibrillary tangles" (twisted fragments of protein within nerve cells that clog up the cell), "neuritic plaques" (abnormal clusters of dead and dying nerve cells, other brain cells, and protein), and "senile plaques" (areas where products of dying nerve cells have accumulated around protein). Although these changes occur to some extent in all brains with age, there are many more of them in the brains of people with AD.

The destruction of nerve cells (neurons) leads to a decrease in neurotransmitters (substances secreted by a neuron to send a message to another neuron). The correct balance of neurotransmitters is critical to the brain.
By causing both structural and chemical problems in the brain, AD appears to disconnect areas of the brain that normally work together.

About 10 percent of all people over 70 have significant memory problems and about half of those are due to AD. The number of people with AD doubles each decade past age 70. Having a close blood relative who developed AD increases your risk.

Early onset disease can run in families and involves autosomal dominant, inherited mutations that may be the cause of the disease. So far, three early onset genes have been identified.
Late onset AD, the most common form of the disease, develops in people 60 and older and is thought to be less likely to occur in families. Late onset AD may run in some families, but the role of genes is less direct and definitive. These genes may not cause the problem itself, but simply increase the likelihood of formation of plaques and tangles or other AD-related pathologies in the brain.
In-Depth Causes »


Symptoms »
In the early stages, the symptoms of AD may be subtle and resemble signs that people mistakenly attribute to "natural aging." Symptoms often include:
Repeating statements
Misplacing items
Having trouble finding names for familiar objects
Getting lost on familiar routes
Personality changes
Losing interest in things previously enjoyed
Difficulty performing tasks that take some thought, but used to come easily, like balancing a checkbook, playing complex games (such as bridge), and learning new information or routines
In a more advanced stage, symptoms are more obvious:
Forgetting details about current events
Forgetting events in your own life history, losing awareness of who you are
Problems choosing proper clothing
Hallucinations, arguments, striking out, and violent behavior
Delusions, depression, agitation
Difficulty performing basic tasks like preparing meals and driving
At end stages of AD, a person can no longer survive without assistance. Most people in this stage no longer:
Understand language
Recognize family members
Perform basic activities of daily living such as eating, dressing, and bathing

In-Depth Symptoms »


Signs and Tests »
The first step in diagnosing Alzheimer's disease is to establish that dementia is present. Then, the type of dementia should be clarified. A health care provider will take a history, do a physical exam (including a neurological exam), and perform a mental status examination.
Tests may be ordered to help determine if there is a treatable condition that could be causing dementia or contributing to the confusion of AD. These conditions include thyroid disease, vitamin deficiency, brain tumor, drug and medication intoxication, chronic infection, anemia, and severe depression.
AD usually has a characteristic pattern of symptoms and can be diagnosed by history and physical exam by an experienced clinician. Tests that are often done to evaluate or exclude other causes of dementia include computed tomography (CT), magnetic resonance imaging (MRI), and blood tests.
In the early stages of dementia, brain image scans may be normal. In later stages, an MRI may show a decrease in the size of the cortex of the brain or of the area of the brain responsible for memory (the hippocampus). While the scans do not confirm the diagnosis of AD, they do exclude other causes of dementia (such as stroke and tumor).

In-Depth Diagnosis »

Unfortunately, there is no cure for AD. The goals in treating AD are to:
Slow the progression of the disease.
Manage behavior problems, confusion, and agitation.
Modify the home environment.
Support family members and other caregivers.
The most promising treatments include lifestyle changes, medications, and antioxidant supplements like vitamin E and ginkgo biloba.

LIFESTYLE CHANGES
The following steps can help people with AD:
Walk regularly with a caregiver or other reliable companion. This can improve communication skills and prevent wandering.
Use bright light therapy to reduce insomnia and wandering.
Listen to calming music. This may reduce wandering and restlessness, boost brain chemicals, ease anxiety, enhance sleep, and improve behavior.
Get a pet dog.
Practice relaxation techniques.
Receive regular massages. This is relaxing and provides social interactions.

DRUG TREATMENT
Several drugs are available to try to slow the progression of AD and possibly improve the person's mental capabilities. Memantine (Namenda) is currently the only drug approved for the treatment of moderate-to-severe Alzheimer’s disease.
Other medicines include donepezil (Aricept), rivastigmine (Exelon), galantamine (Razadyne, formerly called Reminyl), and tacrine (Cognex). These drugs affect the level of a neurotransmitter in the brain called acetylcholine. They may cause nausea and vomiting. Tacrine also causes an elevation in liver enzymes and must be taken four times a day. It is now rarely used.
Aricept is taken once a day and may stabilize or even improve the person's mental capabilities. It is generally well tolerated. Exelon seems to work in a similar way. It is taken twice a day.
Other medicines may be needed to control aggressive, agitated, or dangerous behaviors. These are usually given in very low doses.
It may be necessary to stop any medications that make confusion worse. Such medicines may include pain killers, cimetidine, central nervous system depressants, antihistamines, sleeping pills, and others. Never change or stop taking any medicines without first talking to your doctor.


SUPPLEMENTS
Folate (vitamin B9) is critical to the health of the nervous system. Together with some other B vitamins, folate is also responsible for clearing homocysteine (a body chemical that contributes to chronic illnesses) from the blood. High levels of homocysteine and low levels of both folate and vitamin B12 have been found in people with AD. Although the benefits of taking these B vitamins for AD is not entirely clear, it may be worth considering them, particularly if your homocysteine levels are high.
Antioxidant supplements, like ginkgo biloba and vitamin E, scavenge free radicals. These products of metabolism are highly reactive and can damage cells throughout the body.
Vitamin E dissolves in fat, readily enters the brain, and may slow down cell damage. In at least one well-designed study of people with AD who were followed for 2 years, those who took vitamin E supplements had improved symptoms compared to those who took a placebo pill. Patients who take blood-thinning medications like warfarin (Coumadin) may should talk to their doctor before taking vitamin E.
Ginkgo biloba is an herb widely used in Europe for treating dementia. It improves blood flow in the brain and contains flavonoids (plant substances) that act as antioxidants. Although many of the studies to date have been somewhat flawed, the idea that ginkgo may improve thinking, learning, and memory in those with AD has been promising. DO NOT use ginkgo if you take blood-thinning medications like warfarin (Coumadin) or a class of antidepressants called monoamine oxidase inhibitors (MAOIs).
If you are considering any drugs or supplements, you MUST talk to your doctor first. Remember that herbs and supplements available over the counter are NOT regulated by the FDA.
SUPPORT AT HOME
Someone with AD will need support in the home as the disease worsens. Family members or other caregivers can help by trying to understand how the person with AD perceives his or her world. Simplify the patient's surroundings. Give frequent reminders, notes, lists of routine tasks, or directions for daily activities. Give the person with AD a chance to talk about their challenges and participate in their own care.

OTHER PRACTICAL STEPS
The person with AD should have their eyes and ears checked. If problems are found, hearing aids, glasses, or cataract surgery may be needed.

Those with AD may have particular dietary requirements such as:
Extra calories due to increased physical activity from restlessness and wandering.
Supervised meals and help with feeding. People with AD often forget to eat and drink, and can become dehydrated as a result.

The Safe Return Program, implemented by the Alzheimer's Association, requires that a person with AD wear in identification bracelet. If he or she wanders, the caregiver can contact the police and the national Safe Return office, where information about the person is stored and shared nationwide.
Eventually, 24-hour monitoring and assistance may be necessary to provide a safe environment, control aggressive or agitated behavior, and meet physiologic needs. This may include in-home care, nursing homes, or adult day care.

NY Times Health

"For a perfectly healthy woman, Dianne Kerley has had quite a few medical tests in recent years: M.R.I. and PET scans of her brain, two spinal taps and hours of memory and thinking tests.

Ms. Kerley, 52, has spent much of her life in the shadow of an illness that gradually destroys memory, personality and the ability to think, speak and live independently. Her mother, grandmother and a maternal great-aunt all developed Alzheimer’s disease. Her mother, 78, is in a nursing home in the advanced stages of dementia, helpless and barely responsive.

“She’s in her own private purgatory,” Ms. Kerley said.

Ms. Kerley is part of an ambitious new scientific effort to find ways to detect Alzheimer’s disease at the earliest possible moment. Although the disease may seem like a calamity that strikes suddenly in old age, scientists now think it begins long before the mind fails.

“Alzheimer’s disease may be a chronic condition in which changes begin in midlife or even earlier,” said Dr. John C. Morris, director of the Alzheimer’s Disease Research Center at Washington University in St. Louis, where Ms. Kerley volunteers for studies.

But currently, the diagnosis is not made until symptoms develop, and by then it may already be too late to rescue the brain. Drugs now in use temporarily ease symptoms for some, but cannot halt the underlying disease.

Many scientists believe the best hope of progress, maybe the only hope, lies in detecting the disease early and devising treatments to stop it before brain damage becomes extensive. Better still, they would like to intervene even sooner, by identifying risk factors and treating people preventively — the same strategy that has markedly lowered death rates from heart disease, stroke and some cancers.

So far, Alzheimer’s has been unyielding. But research now under way may start answering major questions about when the disease begins and how best to fight it.

A radioactive dye called PIB (for Pittsburgh Compound B) has made it possible to use PET scans to find deposits of amyloid, an Alzheimer’s-related protein, in the brains of live human beings. It may lead to earlier diagnosis, help doctors distinguish Alzheimer’s from other forms of dementia and let them monitor the effects of treatment.

Studies with the dye have already found significant deposits in 20 percent to 25 percent of seemingly normal people over 65, suggesting that they may be on the way to Alzheimer’s, though only time will tell.

“PIB is about the future of where Alzheimer’s disease needs to be,” said Dr. William E. Klunk, a co-discoverer of the dye at the Alzheimer’s research center at the University of Pittsburgh. “PIB is being used today to help determine whether drugs that are meant to prevent or remove amyloid from the brain are working, so we can find drugs that prevent the underlying pathology of the disease.”

Though PIB is experimental now, studies began in November that are intended to lead to government approval for wider use.

Currently, for the most common form of Alzheimer’s disease, which occurs after age 65, there is no proven means of early detection, no definitive genetic test. But PIB tests might be ready before new treatments emerge, making it possible to predict who will develop Alzheimer’s — without being able to help.

Researchers are also using M.R.I. scans to look for early brain changes, and testing blood and spinal fluid for amyloid and other “biomarkers” to see if they can be used to predict Alzheimer’s or find it early.

Studies of families in which multiple members have dementia are helping to sort out the genetic underpinnings of the disease.

Finally, experiments are under way to find out whether drugs and vaccines can remove amyloid from the brain or prevent its buildup, and whether doing so would help patients. The new drugs, unlike the ones now available, have the potential to stop or slow the progress of the disease. At the very least, the drug studies will be the first real test of the leading theory of Alzheimer’s, which blames amyloid for setting off a chain of events that ultimately ruin the brain.

Some scientists doubt the amyloid theory, but even a staunch skeptic said the studies were important.

Among the skeptics is Dr. Peter Davies, a professor at Albert Einstein Medical College, who said: “You’ve got to try. Somebody’s going to get this right.”

But if the amyloid hypothesis does not hold up, much of Alzheimer’s research could wind up back at Square 1.

Answers are urgently needed. Alzheimer’s was first recognized 100 years ago, and in all that time science has been completely unable to change the course of the disease. Desperate families spend more than $1 billion a year on drugs approved for Alzheimer’s that generally have only small effects, if any, on symptoms. Patients’ agitation and hallucinations often drive relatives and nursing homes to resort to additional, powerful drugs approved for other diseases like schizophrenia, drugs that can deepen the oblivion and cause severe side effects like diabetes, stroke and movement disorders.

Alzheimer’s is the most common cause of dementia (artery disease, Parkinson’s and other brain disorders can also lead to dementia). Five million people in the United States have Alzheimer’s, most of them over 65. It is the nation’s sixth leading cause of death by disease, killing nearly 66,000 people a year and probably contributing to many more deaths. By 2050, according to the Alzheimer’s Association, 11 million to 16 million Americans will have the disease. “Sixteen million is a future we can’t countenance,” said William H. Thies, the association’s vice president for medical and scientific relations. “It will bankrupt our health care system.”

The costs are already enormous, $148 billion a year — more than three times the cost of chronic lung disease, even though Alzheimer’s kills only half as many people. To a great extent, increases in dementia are the price of progress: more and more people are living long enough to get Alzheimer’s, some because they survived heart disease, strokes or cancer. It is a cruel trade-off. The disease is by no means inevitable, but among people 85 and older, about 40 percent develop Alzheimer’s and spend their so-called golden years in a thicket of confusion, ultimately becoming incontinent, mute, bedridden or forced to use a wheelchair and completely dependent on others.

“It makes people wonder whether they really want to live that long,” Dr. Klunk said.

The potential market for prevention and treatment is enormous, and drug companies are eager to exploit it. If a drug could prevent Alzheimer’s or just reduce the risk, as statins like Lipitor do for heart disease, half the population over 55 would probably need to take it, Dr. Thies said.

MORE... New York Times

"

New York Times

By SANDRA BLAKESLEE
Published: April 8, 2008
If Rod Serling were alive and writing episodes for “The Twilight Zone,” odds are he would have leaped on the true story of Anne Adams, a Canadian scientist turned artist who died of a rare brain disease last year.


Trained in mathematics, chemistry and biology, Dr. Adams left her career as a teacher and bench scientist in 1986 to take care of a son who had been seriously injured in a car accident and was not expected to live. But the young man made a miraculous recovery. After seven weeks, he threw away his crutches and went back to school.

According her husband, Robert, Dr. Adams then decided to abandon science and take up art. She had dabbled with drawing when young, he said in a recent telephone interview, but now she had an intense all-or-nothing drive to paint.

“Anne spent every day from 9 to 5 in her art studio,” said Robert Adams, a retired mathematician. Early on, she painted architectural portraits of houses in the West Vancouver, British Columbia, neighborhood where they lived.

In 1994, Dr. Adams became fascinated with the music of the composer Maurice Ravel, her husband recalled. At age 53, she painted “Unravelling Bolero” a work that translated the famous musical score into visual form.

Unbeknown to her, Ravel also suffered from a brain disease whose symptoms were identical to those observed in Dr. Adams, said Dr. Bruce Miller, a neurologist and the director of the Memory and Aging Center at the University of California, San Francisco. Ravel composed “Bolero” in 1928, when he was 53 and began showing signs of his illness with spelling errors in musical scores and letters.

“Bolero” alternates between two main melodic themes, repeating the pair eight times over 340 bars with increasing volume and layers of instruments. At the same time, the score holds methodically to two simple, alternating staccato bass lines.

“ ‘Bolero’ is an exercise in compulsivity, structure and perseveration,” Dr. Miller said. It builds without a key change until the 326th bar. Then it accelerates into a collapsing finale.

Dr. Adams, who was also drawn to themes of repetition, painted one upright rectangular figure for each bar of “Bolero.” The figures are arranged in an orderly manner like the music, countered by a zigzag winding scheme, Dr. Miller said. The transformation of sound to visual form is clear and structured. Height corresponds to volume, shape to note quality and color to pitch. The colors remain unified until the surprise key change in bar 326 that is marked with a run of orange and pink figures that herald the conclusion.

Ravel and Dr. Adams were in the early stages of a rare disease called FTD, or frontotemporal dementia, when they were working, Ravel on “Bolero” and Dr. Adams on her painting of “Bolero,” Dr. Miller said. The disease apparently altered circuits in their brains, changing the connections between the front and back parts and resulting in a torrent of creativity.

“We used to think dementias hit the brain diffusely,” Dr. Miller said.

(click link below foe full story at New York Times)


FTD - Frontotemporal Dementia - Brain Disease - Pick's Disease - Creativity - New York Times

An Alzheimer's disease research paper published last year in a prestigious medical journal failed to disclose the financial ties one of the co-authors had to Elan (ELN - Cramer's Take - Stockpickr) and Wyeth (WYE - Cramer's Take - Stockpickr) as a paid consultant to the drugmakers.

The paper in the September 2007 Archives of Neurology, a journal published by the American Medical Association, describes the use of a new test -- the neuropsychological test battery (NTB) -- to measure the memory and mental status of patients with Alzheimer's disease.

John Harrison, the consultant, was paid by Elan and Wyeth to create the NTB as a new cognitive test for the company's experimental Alzheimer's drug, bapineuzumab. As previously reported by TheStreet.com, Elan and Wyeth are seeking to convince regulators here and in Europe that the NTB should be used as the basis to approve bapineuzumab.

The NTB, the companies have argued, is a superior alternative to the ADAS-cog test, the most well-known and widely used measure of cognition in studies of mild to moderate Alzheimer's patients today.

To help make their point, Elan and Wyeth have cited the Archives of Neurology paper, titled "A Neuropsychological Test Battery for Use in Alzheimer Disease Clinical Trials," as independent, scientific proof that validates the NTB.

Harrison is the lead author of that NTB paper, but his role as a consultant paid by Elan and Wyeth to create the test is not disclosed in it. Harrison is the only author of six listed in the paper's conflict-of-interest statement as having no financial conflicts with Elan and Wyeth. Harrison's five co-authors are all employed by Elan or Wyeth.

"The drafts of our manuscript specifically included reference to the fact that I had received payment from both Elan and Wyeth, though for some reason this disclosure does not appear in the published manuscript," said Harrison in an email response to questions.

"This is clearly worthy of further investigation, and I will seek to discover why this statement was omitted," he added.

Why Does Full Disclose Matter?

Studies have shown that when drug companies or an industry fund scientific research, the conclusions of that research tend to favor those who pay for it. This is why independent research is so highly valued and why, when drug companies are involved in the conduct or payment of research, proper financial disclosure is necessary...CLICK BELOW FOR FULL STORY

Elan and Wyeth Had Ties to Study's Authors | Drugs


- TheStreet.com

DURHAM, N.C., Dec. 17 -- Walking briskly for 30 minutes a day, six days a week, can significantly reduce blood pressure, waist circumference, triglycerides, and fasting glucose, while increasing HDL, according to researchers here. Action Points
Explain to interested patients that this study confirms earlier reports of the benefit of moderate amounts of daily exercise.

Compared with sedentary adults, those with moderate intensity exercise -- walking 10 to 11 miles over an average 170 minutes a week -- resulted in a significant improvement in metabolic syndrome

By Judith Groch, Senior Writer, MedPage Today

BIRMINGHAM, Ala., Nov. 13 -- The simple expedient of giving glasses to nursing home residents to correct refractive error improved their quality of life and decreased depression, according to researchers here.

Rates of vision impairment for nursing home residents in the U.S. are three to 15 times higher than rates for community-dwelling older adults, Cynthia Owsley, Ph.D., of the University of Alabama at Birmingham, and colleagues wrote in the November issue of Archives of Ophthalmology.

Yet, the researchers said, national surveys have found that only half of nursing homes in the U.S. report having contracts for vision and hearing services, and only 12.6% of nursing homes have optometric services available on site.

To examine the effect of providing glasses for nursing home residents with uncorrected refractive error (myopia, hyperopia, and presbyopia), the researchers undertook a study of 142 such patients, ages 55 or older.

Of these, 78 were randomly assigned to immediate correction with glasses, while 64 were randomized to delayed correction after a two-month follow-up visit. The average age of participants (75% women) was in the late 70s. The residents had an average of five to six chronic medical conditions, and about two-thirds had a diagnosis of a cataract.

They had uncorrected refractive error in one or both eyes for near or far test distances as determined by routine eye examination. Individuals were assessed at baseline and at two-month follow-up.

Distance visual acuity was assessed with the ETDRS chart, while near visual acuity was assessed with the Lighthouse Near Visual Acuity Test (modified ETDRS).

For quality of life, the researchers used the Nursing Home Vision-Targeted Health-Related Quality-of-Life Questionnaire (NHVQoL), which consisted of nine subscales focusing on general vision, reading, ocular symptoms, mobility, psychological stress, activities of daily living, activities and hobbies, adaptation and coping, and social interaction.

Two other questionnaires were used to assess generic health-related quality of life (physical and mental components), and the VF-14 to assess visual activities of daily living.

Depressive symptoms were assessed by the 15-item Geriatric Depression Scale.

At baseline, both groups had similar demographic and medical characteristics and had similar visual acuity and refractive error uncorrected by eyeglasses.

At two months, the immediate correction group compared with the delayed group had higher scores on the NHVQoL subscales for reading, psychological distress, activities and hobbies, and social interaction (all P<0.04)>

They also had fewer depressive symptoms as measured by the Geriatric Depression Scale (P=0.003).

Overall, the researchers said that after providing glasses, intervention scores on the NHVQoL subscales increased dramatically, reaching about 12 points for general vision and reading, with other subscales showing more modest increases of about five points.

Because the average level of uncorrected refractive error at baseline was ± 1.00 D for distance and + 1.25 D for near, these results show that improvement of even modest to moderate levels of optical defocus can benefit the health and well-being of nursing home residents, the investigators said.

Compared with those who did not receive new glasses, residents who received new spectacles not only rated the overall quality of general vision more highly but also reported less difficulty with reading (newspapers, books, wall clocks) and with the performance of activities and hobbies such as writing, using the phone, watching TV, and playing cards.

Optical correction also enhanced psychological well-being. Benefits included less reported psychological distress (worry, frustration, upset), increased social interaction (visiting with fellow residents in their rooms, participating in group activities), and fewer depressive symptoms.

Nursing home residents are at increased risk for depression, which in turn increases their mortality risk over a year. With prevalence estimates in the nursing home for major depression ranging as high as 43%, interventions that successfully reduce depressive symptoms in this population are significant, Dr. Owsley's team said.

Noting the study's limitations, the investigators said that generalizability of conclusions beyond two months of follow-up and to nursing home residents in other geographic areas remains unknown. Also, the study could not address the efficacy of spectacle intervention for nursing home residents with a Mini-Mental State Examination score (MMSE) less than 13.

These findings underscore the need for a systematic evaluation of the factors underlying the pervasive unavailability of eye care for nursing home residents in the U.S., so that steps can be taken to improve service delivery and eye care utilization, the researchers concluded.

Triple Therapy Leads to Lasting Improvement in Macular Degeneration
By Charles Bankhead, Staff Writer, MedPage Today


NEW ORLEANS, Nov. 13 -- For many patients with choroidal neovascularization from age-related macular degeneration, a single cycle of photodynamic therapy, bevacizumab (Avastin), and intravitreal steroids led to sustained improvement in visual acuity, German investigators reported here.

After a mean follow-up of 62 weeks, improvement in visual acuity for 104 eyes in 104 patients averaged 2.1 lines (P<0.01),>

Retinal thickness also decreased significantly (P<0.01).

Triple therapy was well tolerated, no severe systemic or optical adverse effects occurred, and intraocular pressure did not increase, he added.

"Ultimately, we must tailor therapy to suit the individual's disease characteristics, ability to visit the clinic, and treatment preference or feasibility," Dr. Augustin concluded.

Age-related macular degeneration has a multifactorial pathogenesis that involves hypoxia, oxidative pressure, inflammatory responses, and an altered balance of pro- and antiangiogenic factors that results in neovascularization, Dr. Augustin noted. An ideal therapy, he said, would include an antiangiogenic agent, an anti-inflammatory, and photodynamic therapy to treat existing choroidal neovascularization.

Dr. Augustin and colleagues have used triple therapy in more than 400 patients, and he reported results for patients who have been followed the longest. Treatment consisted of 70-second photodynamic therapy with verteporfin, followed an average of 16 hours later by intravitreal administration of 800 µg of dexamethasone and 1.5 mg of bevacizumab.

In addition to the improvement in visual acuity, retinal thickness decreased by an average of 195 µm. Five patients required a second cycle of therapy because of persistent choroidal neovascularization activity. Additionally, 23 patients (22%) received a second injection of bevacizumab.

The triple therapy results in significant and sustained improvement in visual acuity, has a good safety profile, is convenient for patients, and is cost-effective over time as compared with indefinite therapy, such as an anti-VEGF agent, Dr. Augustin concluded.

Active Men Lessen Later Fracture Risk - CME Teaching Brief® - MedPage Today

UPPSALA, Sweden, June 19 -- Osteoporotic fracture may be less common among men than women, but a lifetime of physical activity appears to be just as important in reducing this risk, researchers found. Action Points

Explain to interested patients that this study suggests that men appear to gain protection against hip and other fractures by physical activity.

Inform patients that increasing physical activity, even in later life, appears to further reduce fracture risk.

Fragility hip fractures were more than twice as common among men who reported little recreational exercise during 35 years of follow-up as among those who participated in sports at least three hours a week, found Karl Michaëlsson, M.D., Ph.D., of University Hospital here, and colleagues in a longitudinal study.

One-third of all hip fractures among men could be prevented by regular participation in sports, they wrote online in the journal PLoS Medicine.

This finding "is fully concordant with a similar analysis in women," noted Harri Sievänen, Ph.D., and Pekka Kannus, M.D., Ph.D., both of the UKK Institute in Tampere, Finland, in an accompanying editorial.

For postmenopausal women, moderate exercise has been shown to substantially lower hip fracture risk. For men, though, prospective observational studies have had inconsistent results.

"Given these inconsistent findings, the results … represent an important advance," Drs. Sievänen and Kannus wrote.

Dr. Michaëlsson and colleagues analyzed the physical activity component of the Uppsala Longitudinal Study of Adult Men, which surveyed 2,205 men in the city who were ages 49 to 51 when the study began in the early 1970s.

At baseline and at age 60, 70, 77, and 82 the participants completed questionnaires asking about how they spent their leisure time.

Half reported that they engaged in active sports or heavy gardening for at least three hours a week, or regularly engaged in hard physical training or competitive sports, collectively defined as high physical activity.

Another 36.4% were included in the intermediate activity category for responding that they "often" went walking or cycling for pleasure.

Only 14.7% reported spending their leisure time in mostly sedentary activities.

The men were followed for fracture using Sweden's national Hospital Discharge Register and local hospital registers and records.

During the 35-year follow-up, 482 men (22%) experienced a fracture of some type and 134 (6%) had a hip fracture. [CLICK HERE TO READ ENTIRE ARTICLE]

AAICPD: Low-Tech Tool Predicts Six-Year Risk of Dementia - CME Teaching Brief® - MedPage Today

WASHINGTON, June 11 -- The risk of developing dementia within six years can be predicted by a simple assessment tool that relies on clinical impression and patient history, researchers reported here. Action Points

Explain to interested patients that this report describes an assessment tool that has not been tested in a large randomized trial.

This report is based upon material published as an abstract and presented at a meeting. It has not been published in a peer-reviewed journal.
The key indicators were older age, non-white race, poor cognitive function, poor physical performance, extreme inactivity, history of bypass surgery, low body mass index, and lack of alcohol consumption (ROC, 0.79; 95% CI: 0.76 - 0.81; accuracy, 87%), said Deborah F. Barnes, Ph.D., of the University of California San Francisco.

The score based on these factors ranged from 0 to 14 points, and the risk of developing dementia was 6% in those with low scores (0-3 points), compared with 25% in those with moderate scores (4-6 points), and 54% in patients with high scores (≥7), she reported at the Alzheimer's Association International Conference on Prevention of Dementia.

Moreover, evaluation of these factors can be performed in a physician's office or at bedside in a hospital by a nurse practitioner or a physician's assistant, Dr. Barnes found.

She noted that this low-tech model was not as accurate as one that incorporates MRI and other expensive tests. By statistical analysis the high-tech model was significantly better (P<0.001), but the "absolute differences between the two was small."

"We wanted a tool that could be used quickly in a clinical setting and wouldn't require expensive or sophisticated measures, like MRI," she said in an interview. "We looked at a number of potential predictors and settled on these as a reasonable model that a clinician could use when evaluating an older adult."

On the basis of an analysis of data from 3,375 non-demented participants in the Cardiovascular Health Cognition Study, Dr. Barnes and colleagues developed the two models -- a bedside predictive protocol and the so-called best predictive model. At baseline, participants had a mean age of 76; 59% were women, and 15% were African American.

Fourteen percent (480) of those in the analysis developed dementia over six years of follow-up.

The best model included testing for apolipoprotein-E genotype, MRI findings, electrocardiogram findings, carotid artery ultrasound, and ankle-arm brachial index, as well as demographics, medical history, psychosocial measures, physical function, cognitive function, self-rated health and medication use.

Dr. Barnes said the simple protocol can be used to aid in evaluation of "elderly patients about whom the clinician may have some concerns or patients whose family members raise concerns about performance or ability to live independently."

Unlike cardiovascular disease or diabetes in which elevated risk triggers preventive measures, including pharmacologic interventions, Dr. Barnes conceded that little is known about preventing dementia, which also raises questions about the value of a predictive model.

She agreed that there are no medications that have been shown to reduce the risk of dementia, but said there are a number of compounds under development "so it may be that we will soon have drugs that can be used in patients who have an identified increased risk."

Additionally, she said that several studies have suggested lifestyle interventions, specifically both mental and physical exercise, that have been associated with a reduced risk of dementia.

"It would be reasonable to initiate both an exercise program and a program of mental drills or exercises such as word puzzles in patients who are identified as high risk for dementia," she said.

Elderly Pa. Women Pose For Risque Photos

(AP) GREENSBORO, Pa. Giving sultry looks and sexy smiles to the camera, 12 Pittsburgh-area women recently posed at Monongahela historical sites, baring it all -- or almost all -- to create a charity-driven calendar. The catch?

The nearly nude ladies are all in their 70s and 80s, driven to adventure by a desire to raise money for a historical society in Monongahela, a small community 17 miles southeast of Pittsburgh.

Overcoming fears the priest would walk by during a photo shoot or embarrassing their children and grandchildren, the women -- all well-known members of the tight-knit community -- are now eagerly awaiting the calendar's debut next month. The money it generates will go to the Monongahela Area Historical Society.

"One of the advantages of being old is that you can do anything you want and get away with it," said 80-year-old Lois Phillips, who as Miss September was photographed in the back seat of a 1968 Mercury convertible.

The calendar was the brainchild of 80-year-old Lorys Crisafulli. She came up with the idea when she saw the movie Calendar Girls, a 2003 flick starring Helen Mirren in which a group of British women publish a nude calendar to raise money for cancer research.

"I thought, why don't we do that in Monongahela?" she told the Pittsburgh Post-Gazette. "We need something to put us on the map, to get us going."

Crisafulli spent the next few weeks finding sponsors, a free photographer and an eager group of septuagenarians and octogenarians with enough spunk to show some flesh.

A former 5th grade teacher, Crisafulli is about to become better known as Miss January, who lounges in a black convertible covered in pearls, holding a champagne glass in one hand and dangling slinky sandals from the other.

Some of the other photos are more risque.

Miss April, Esther Cox, poses in a pasture, nothing but a pink umbrella covering her 75-year-old body. Miss December, Sondra Odelli Bordini, gives a sultry glance from behind a poinsettia centerpiece with two strategically placed red Christmas balls.

New Drugs Cool Rheumatoid Arthritis Flames - CME Teaching Brief® - MedPage Today

VIENNA, June 13 -- Three drugs, two approved and one in the pipeline, are improving care for patients with severe rheumatoid arthritis (RA) according to clinicians here. Action Points

Explain that patients with severe rheumatoid arthritis have varying responses to anti-inflammatory drugs and disease-modifying antirheumatic drugs, and that they may respond to drugs differently than other patients with RA.
The three agents -- rituximab (Rituxan), abatacept (Orencia), and toclizumab (Acterma) -- all reduce signs and symptoms of RA, improve physical function and health status, and slow joint damage progression, said Josef S. Smolen, M.D., of the Medical University of Vienna, and colleagues.

The heterogeneity of the disease is one of the reasons why no single therapy is effective for all patients or for one patient at all times, the authors wrote in a review article published in the online edition of The Lancet.

Disease-modifying anti-rheumatic drugs such as the anti-tumor necrosis factor (TNF) agents etanercept (Enbrel), infliximab (Remicade), and adalimumab (Humira), in combination with methotrexate, have significant anti-inflammatory and joint-protecting activity, they noted.

Yet, they noted, the combination of a TNF antagonist and methotrexate is better at protecting against radiographically confirmed progression of joint damage in patients with low disease activity than in patients with highly active disease.

To see if there might be relief for those patients, the investigators reviewed the action, efficacy, and safety of the three newer agents, each of which has a mechanism of action different from that of established anti-arthritis agents.

Rituximab, an anti-CD20 antibody with proven efficacy in the treatment of both rheumatoid arthritis and B-cell non-Hodgkin's lymphoma, is approved in the U.S. and Europe for treatment of rheumatoid arthritis in patients who have failed TNF-inhibitor therapy.

"The rationale for use of rituximab in treatment of this disease comes from the fact that B cells have several functions in disease pathogenesis, including antigen presentation and (auto)antibody and cytokine production," the investigators wrote. "Although rituximab leads to considerable reduction of concentrations of rheumatoid factor, the mechanism of action in rheumatoid arthritis is not clear."

In clinical trials, rituximab was associated with reduction in rheumatoid arthritis symptoms by more than 50% for more than a third of patients. Although the drug rapidly depleted B cells in all clinical trials, with an effect lasting for more than six months in most cases, the disease flares up again as B cells repopulate, and retreatment is necessary to maintain efficacy, the authors noted. CLICK HERE TO READ ENTIRE ARTICLE

Better Education Spurs Alzheimer's Patients to Try Risky Treatments

SUNDAY, June 10 (HealthDay News) -- Alzheimer's disease patients who have a better understanding of their condition seem to be more willing to accept potentially risky treatments, a U.S. study finds.

Researchers at the University of Pennsylvania interviewed 34 people with mild to moderate Alzheimer's who lived in the community. The patients were asked if they would want to take medications that would delay the progression of Alzheimer's for one year. The patients were told the risk of the treatments ranged from a 30 percent chance of pain to a 10 percent chance of death.

Patients with more insight into their symptoms, diagnosis and prognosis were generally more risk-tolerant, the study found. Patients who were willing to accept increased risk also were more likely to be judged competent to make a treatment decision and more capable of analyzing the risks, benefits and purpose of a medication.

"From the patient perspective, the willingness to take a risky Alzheimer's treatment is more driven by their awareness of their illness and their capacity to understand, appreciate and reason through a treatment's purpose, benefits and risks to themselves, and not so much on the severity of their Alzheimer's disease," study author Jason Karlawish, an associate professor of medicine and associate director of the university's Memory Center, said in a prepared statement.

The study was to be presented at the Alzheimer's Association International Conference on Prevention of Dementia, in Washington, D.C.

This type of research may help drug companies, doctors and regulatory agencies better understand Alzheimer's patients' willingness to accept risky treatments, he said.

Karlawish noted that several treatments currently being tested may "present more than minimal risks to patients. For example, researchers had to stop one of the early studies of the anti-amyloid vaccination because subjects developed encephalitis, a dangerous inflammation of the brain."

In a second study presented at the conference, researchers conducted an Internet survey of 2,146 Americans, aged 60 and older. They found they were willing to accept a 46.8 percent increase in the risk of death or disability for treatments that would prevent mild Alzheimer's from progressing to more serious stages.

"This survey is the first to our knowledge that is able to quantify this fear of Alzheimer's in a manner that could be useful to health authorities as they plan for the increase in Alzheimer's brought on by the aging of our population," study author Reed Johnson, senior fellow and principal economist at RTI Health Solutions, said in a prepared statement.


More information
The Alzheimer's Association outlines treatment options for Alzheimer's disease.

At the 2007 Alzheimer's Association International Conference on the Prevention of Dementia - Neurochem's U.S. Principal Investigator Presents Update on Tramiprosate
(ALZHEMED(TM))
Monday June 11, 5:55 am ET


WASHINGTON, DC, June 11 /CNW Telbec/ - Paul S. Aisen, M.D., Professor of Neurology and Medicine at Georgetown University Medical Center, and principal investigator in the United States of Neurochem Inc.'s North American Phase III clinical trial for tramiprosate (ALZHEMED(TM)) will present today an update on Neurochem's investigational product candidate for the treatment of Alzheimer's disease (AD). The presentation by Dr. Aisen will take place at the Intervention and Treatment Session, scheduled from 2:30 - 4:30 P.M. (ET), at the Alzheimer's Association International Conference on Prevention of Dementia in Washington, DC. In his presentation entitled, A Phase III Study of the Efficacy, Safety and Disease Modification Effect of Tramiprosate in Mild-to-Moderate Alzheimer's Disease, Dr. Aisen will review the Phase III clinical trial and provide an update.

Neurochem announced in April 2007 that an adjustment to the initial statistical model, as set out in the statistical plan, would be necessary to provide accurate results. The procedure to arrive at a reliable model involves a detailed analysis of potential confounding factors, and Dr. Aisen will present on the progress to date. In addition, Dr. Aisen will provide an update on the progress in the analysis of the Phase III clinical trial primary endpoint data. Some preliminary descriptive data shows numerical differences in favor of tramiprosate (ALZHEMED(TM)) on the primary clinical endpoint and also shows differences between groups on the primary disease modification endpoint as measured by magnetic resonance imaging (MRI). However, work regarding the adjustment of the statistical model is ongoing and, therefore results of the Phase III clinical trial cannot be derived from the preliminary data nor can statistical significance be assigned at this time. Accordingly, no predictions or conclusions can yet be made regarding the outcome of the Phase III study.

Neurochem continues to expect to announce the top-line results of the trial during the second quarter of this year, although they may not be available within this timeframe. The actual timing of the release of these top-line results depends on completing the adjustments to the initial statistical model.

Alzheimer's Association News Briefing

The Alzheimer's Association has invited Dr. Aisen to present on the tramiprosate (ALZHEMED(TM)) program for inclusion in a news briefing to be held today, June 11, 2007, at 12:00 P.M. (ET).

Continuing Medical Education Symposium

Neurochem is also supporting a CME symposium on June 11 at 6:30 PM at the conference. The symposium, entitled Confronting the Burgeoning AD Crisis: New Frontiers, is sponsored by Professional Postgraduate Services(R). The invited faculty presenters are Howard M. Fillit, MD, Steven T. DeKosky, MD and Serge Gauthier, MD, and they will examine the burden of AD and assess the need for improving diagnosis, with a special focus on shifting the treatment paradigm from managing symptoms to treating the underlying causes of the disease.

Neurochem Poster Presentations

Neurochem is also exhibiting three poster presentations on tramiprosate (ALZHEMED(TM)) at this conference. All posters are displayed in the Exhibit Hall of the Marriott Wardman Park Hotel, open on June 10 from 10:30 A.M. to 6:30 P.M. (ET) and on June 11 from 9:30 A.M. to 4:30 P.M. (ET).


- Presentation P-187, entitled Tramiprosate Is Neuroprotective and
Reduces the Levels of Secreted Amyloid-ss in Organotypic Hippocampal
Slice Cultures, will be presented by lead author Mounia Azzi.
- André Galarneau will present GABA-Dependent Pathways in the
Neuroprotective Effect of Tramiprosate against Amyloid-ss Toxicity
in presentation P-190.
- Barry D. Greenberg will present Tramiprosate Decreases Amyloid-ss
Induced Erk1/2 Activity in Primary Rat Neurons by a GABA-Independent
Pathway in presentation P-192.

About Neurochem

Neurochem Inc. is focused on the development and commercialization of
innovative therapeutics to address critical unmet medical needs. Eprodisate
(KIACTA(TM)) is currently being developed for the treatment of Amyloid A (AA)
amyloidosis, and is under regulatory review for marketing approval by the
United States Food and Drug Administration, European Medicines Agency and
Swissmedic. Tramiprosate (ALZHEMED(TM)), for the treatment of Alzheimer's
disease, has completed a Phase III clinical trial in North America and is
currently in a Phase III clinical trial in Europe, while tramiprosate
(CEREBRIL(TM)), for the prevention of Hemorrhagic Stroke caused by Cerebral
Amyloid Angiopathy, has completed a Phase IIa clinical trial.

To Contact Neurochem

For additional information on Neurochem and its drug development programs,
please call the North American toll-free number 1 877 680-4500 or visit our
Web Site at: www.neurochem.com.

This news release contains forward-looking statements regarding
tramiprosate (ALZHEMED(TM)) as well as regarding continuing and further
development efforts. These statements are based on the current analysis and
expectations of management. Drug development necessarily involves numerous
risks and uncertainties, which could cause actual results to differ materially
from this current analysis and these expectations. Analysis regarding the
results of clinical trials may not provide definitive results regarding
safety, tolerability or therapeutic benefits. Even if all the endpoints sought
in the clinical trials were met (which is not certain), there is no certainty
that regulators would ultimately approve tramiprosate (ALZHEMED(TM)) for sale
to the public. Risks and uncertainties may include: failure to demonstrate the
safety, tolerability and efficacy of our product, that actual results may vary
once the final and quality-controlled verification of data and analyses has
been completed, the expense and uncertainty of obtaining regulatory approval,
including from the FDA, and the possibility of having to conduct additional
clinical trials. Further, even if regulatory approval is obtained, therapeutic
products are generally subject to: stringent on-going governmental regulation,
challenges in gaining market acceptance, and competition. Neurochem does not
undertake any obligation to publicly update its forward-looking statements,
whether as a result of new information, future events, or otherwise. Please
see the Annual Information Form for further risk factors that might affect the
Company and its business.

For further information

Lise Hébert, PhD, Vice President, Corporate Communications, (450) 680-4572, lhebert@neurochem.com

Medivation Alzheimer's Data Show Benefit
Monday June 11, 7:53 am ET
Medivation Study Shows Dimebon Benefit in Treatment of Alzheimer's Disease


NEW YORK (AP) -- Biotech drug developer Medivation Inc. said Monday its Alzheimer's treatment Dimebon significantly improved symptoms of the disease over one year.
The mid-stage clinical trial found that patients with mild-to-moderate Alzheimer's disease given Dimebon showed benefits in cognition, overall clinical function, activities of daily living, and behavioral problems compared with those patients given a placebo.

The company also noted that benefits from Dimebon at one year were stable or greater compared to benefits at six months.

The Alzheimer's Association estimates that about 26.6 million people had the disease in 2006, with researchers predicting that the number will jump to more than 100 million by 2050 worldwide.

Neuro-Hitech, Inc. (NHPI) Completes Patient Enrollment for U.S. Phase II Clinical Trial of Huperzine A
Jun 11 2007, 8:31 AM EST
Business Wire


Neuro-Hitech, Inc. (NASDAQ: NHPI) today announced that its U.S. Phase II clinical trial of Huperzine A is fully enrolled. In December 2006, a decision was made to increase enrollment from the original target of 150 by an additional 60 patients. Enrollment was recently concluded with 210 subjects at 35 trial sites throughout the U.S.

This Phase II clinical trial of Huperzine A is a randomized, placebo-controlled study designed to evaluate the compound's safety and efficacy in improving cognitive function of Alzheimer's patients. The study design used a three parallel-arm approach, meaning that patients are randomly assigned into one of three equally sized groups. Each group is administered either Huperzine A twice daily in an escalating 200mcg dose, Huperzine A twice daily in an escalating 400 mcg dose, or a placebo. The study is 24 weeks in length with the primary end-point being the ADAScog score at 16 weeks. After 24 weeks, patients are offered the option to participate in an open label extension for up to a total of 32 weeks while placebo patients are offered active drug at 16 weeks.

The Phase II trial of Huperzine A has been supported by some of the notable researchers and organizations in the Alzheimer's disease community. Dr. Paul Aisen, Professor of Neurology and Medicine at Georgetown University and one of the first clinicians to conduct formal trials in Alzheimer's disease, is the lead investigator for this trial. The National Institutes of Health (NIH) and the Alzheimer's Disease Cooperative Study (ADCS) have also been influential in the conduct of this important clinical trial.

Mr. Reuben Seltzer, Chief Executive Officer of Neuro-Hitech commented, "The entire management team is pleased that enrollment has closed in the Phase II trial of Huperzine A. Because of support from Dr. Paul Aisen, the National Institute of Health, the Alzheimer's Disease Cooperative Study and many others, this trial has been executed flawlessly."

About Neuro-Hitech, Inc.

Neuro-Hitech, Inc. is a New York-based biopharmaceutical company focused specifically on the development and commercialization of next-generation therapies against proven targets for neurodegenerative diseases. Our lead product candidate, Huperzine A, is being clinically tested for efficacy and safety in the treatment of Alzheimer's disease. Huperzine A has been shown to protect nerve cell death and have a longer duration of acetylcholinesterase inhibitory action relative to other cholinesterase inhibitors. In addition to Huperzine A, Neuro-Hitech has two major preclinical development programs. One consists of a portfolio of second-generation anti-amyloid compounds that target A-beta and Tau proteins. The other targets the development of a novel series of compounds designed to treat (anti-ictogenic) and prevent (anti-epileptogenic) epilepsy.

Find more information about Neuro-Hitech online at www.neurohitech.com.

FORWARD-LOOKING STATEMENTS

This press release contains forward-looking statements (as defined in Section 27A of the Securities Act and Section 21E of the Exchange Act). To the extent that any statements made in this press release contain information that is not historical, these statements are essentially forward-looking. Forward-looking statements can be identified by the use of words such as "expects," "plans," "will," "may," "anticipates," "believes," "should," "intends," "estimates," "projects" and other words of similar meaning. These statements are subject to risks and uncertainties that cannot be predicted or quantified and, consequently, actual results may differ materially from those expressed or implied by such forward-looking statements. Such risks and uncertainties include those outlined in "Risk Factors" found within our Annual Report on Form 10-KSB and include, without limitation, Neuro-Hitech's limited cash and ability to raise capital to finance the growth of Neuro-Hitech's operations, the ability of Neuro-Hitech to develop its products and obtain necessary governmental approvals, Neuro-Hitech's ability to protect its proprietary information, Neuro-Hitech's ability to attract or retain qualified personnel, including scientific and technical personnel and other risks detailed from time to time in Neuro-Hitech's filings with the SEC, or otherwise.

Unexplained Late-life Weight Loss May Be Early Predictor Of Alzheimer's Disease
Science Daily — New findings show unexplained weight loss that precedes dementia by more than 10 years is associated with the severity of Alzheimer changes in the brain.

Using data from the Nun Study, a prospective study of the causes of dementia in Catholic sisters, University of South Florida researcher James Mortimer, PhD, reported today that the most likely cause of the unexplained weight loss is the severity of the Alzheimer changes in the brain rather than an eating disorder or other condition associated with declining cognition. Dr. Mortimer presented the findings at the Alzheimer's Association International Conference on the Prevention of Dementia in Washington, DC.

Although a previous study showed that individuals with lower weight for their height at the time of death had more Alzheimer brain changes at autopsy, this is the first study to show that lower weight up to 10 years earlier is specifically related to the severity of the disease.

"While weight one year or less prior to death was related to the amount of cognitive decline, this association could be explained by the severity of the Alzheimer process in the brain seen at autopsy," said Dr. Mortimer, professor of epidemiology at the USF College of Public Health.

"Given its very long duration prior to onset of dementia, it is likely that weight loss is specifically associated with the Alzheimer disease process and not to a restriction in food intake due to cognitive decline," he said. "There is considerable evidence that Alzheimer changes in the brain precede the first symptoms of this illness by decades."

Unexplained weight loss late in life, when coupled with other biomarkers, may help to identify those at risk of Alzheimer's disease more than a decade in the future. Identification of individuals who are at high risk of Alzheimer's long before cognitive decline becomes evident will be critical to its prevention once agents become available to slow the disease, Dr. Mortimer said.

The Nun Study, begun in 1992, is a study of 678 Catholic sisters, initially 75 to 102 years of age, who are evaluated yearly and who agreed to brain donation at the time of death. The Nun Study is directed by Dr. David Snowdon of the University of Kentucky. Dr. Snowdon is a co-author of the presentation as is Dr. William Markesbery, director of the Sanders-Brown Center on Aging at the University of Kentucky. Dr. Yougui Wu, the third coauthor, is an assistant professor of epidemiology and biostatistics at the USF College of Public Health

The Nun Study is funded by a grant from the National Institute on Aging.

Note: This story has been adapted from a news release issued by University of South Florida Health.

CLICK HERE TO READ ENTIRE ARTICLE

IN the book “Mrs. Frisby and the Rats of NIMH,” a group of lab rats acquire human intelligence through a genetic experiment. Every child recognizes the charming tale as pure fantasy, yet something similar is occurring at a major pharmaceuticals company, Wyeth, where rodents tested in its labs have, indeed, taken on some features of the human brain.

Unlike the fictional rats that learned to read, write and operate machinery, Wyeth’s animals are slow-witted, confused and forgetful because they suffer from the crippling dementia of Alzheimer’s disease, which they acquired from a transplanted human gene.

Something else extraordinary is going on at Wyeth. The company’s scientists not only can give rodents Alzheimer’s — they have also figured out how to take it away. Curing mice is a lot simpler than curing people, but the results are a tantalizing development that offers hope to humans suffering from the disease. The work also advances what Wyeth executives describe as their war on Alzheimer’s.

Wyeth’s team faces a formidable foe. In an industry often criticized as making pricey “me too” drugs that involve minor tweaks to competitors’ products, as well as promoting medicines of marginal value, Wyeth has decided to go full bore against Alzheimer’s, a disease that has defied effective treatment since it was first identified a century ago. The company has dedicated more than 350 scientists exclusively to Alzheimer’s research, and they are working on 23 separate projects for medicines to possibly treat the disease.

About five million people in the United States are living with Alzheimer’s, according to the Alzheimer’s Association, an advocacy group funded by individual donors as well as foundations and major corporations, including drug makers. Without a cure or new treatments, the number of those with the disease could grow to 13.2 million by 2050, the National Institute on Aging estimates.

“I think this is going to be the disease, and maybe one of the biggest health care political issues of my generation,” says Robert Essner, 59, Wyeth’s professorial chief executive. “It’s hard for anyone to envision how to provide health care in the United States if you’re going to have to deal with the burden. You just start to add up the cost, 20 years from now as my generation gets old — it’s phenomenal.”

Mr. Essner will have more than a host of grateful baby boomers awaiting him if Wyeth’s crusade is successful. The company could snare a big financial payoff from what still amounts to a risky bet, one that has already cost Wyeth about $450 million in research funds. But with a treatment that slows progress of the disease possibly selling at more than $20,000 a year, the company’s Alzheimer’s program is one reason that some analysts are voicing renewed enthusiasm about Wyeth’s stock, which had been weighed down for years by costly fen-phen diet drug litigation.

Wyeth is hardly the only company looking for Alzheimer’s treatments. Virtually every large drug maker and a number of smaller biotechnology companies are working to develop Alzheimer’s drugs, with several hundred ideas under study. Several companies are expected to announce results of clinical studies during an international Alzheimer’s meeting that is under way in Washington. “There seems to be a current of excitement,” said Peter Davies, a biochemist at the Albert Einstein College of Medicine in the Bronx, who has studied Alzheimer’s for 30 years. Dr. Davies is working with Eli Lilly and Applied NeuroSolutions on a possible course of treatment that is such a secret that he will not say anything about it. “I wouldn’t say it’s a race,” Dr. Davies said, “but this is novel and we want to get a jump on therapeutics.”

The four Alzheimer’s treatments now on the market work by regulating the action of chemical neurotransmitters in the brain. The drugs — Aricept by Eisai and Pfizer, Exelon by Novartis, Razadyne by Johnson & Johnson and Namenda by Forest Laboratories — have shown mixed results treating Alzheimer’s symptoms and do nothing to stop the disease’s progress.
Dr. Todd Golde, professor of neuroscience at the Mayo Clinic, says that the drugs are not very effective, and that consumers’ large expenditures for them — about $1.4 billion in the United States alone last year, according to data from Verispan — reflect the desperation of patients and their families to treat the disease.

“It’s scary if you look at the trials that got these drugs approved,” Dr. Golde said. “The change in mental status was so small, the average caregiver of a patient would have no way of knowing there was any difference.” While there is no evidence that any of the drugs stem the underlying disease, they were approved based on studies showing temporary improvement or stabilization in some patients with Alzheimer’s. The changes can be as minor as a better ability to dress oneself or to take out the trash.

In one study of people taking Namenda and Aricept combined for six months, 60 percent of patients either improved or did not deteriorate. “I would say that physicians do believe these drugs are of benefit to patients with Alzheimer’s,” said Stephen M. Graham, senior director of clinical development at Forest.

Spokesmen for the other companies with Alzheimer’s drugs echoed that assessment in regard to their products, pointing to clinical studies demonstrating that they help patients.
Wyeth is wagering that it can find more promising treatments for a nebulous, stealthy disease that does more than rob people of their health and well-being. It also steals some of their most precious memories.

AT first blush, Robert Essner seems an unlikely flag bearer for a corporate assault on Alzheimer’s. The son of a college professor, Mr. Essner studied humanities as an undergraduate and in graduate school, intending to teach college history. But after he graduated from the University of Chicago in 1971 with a master’s degree in history, he soon realized that jobs in his field were scarce. He says he stumbled into pharmaceuticals by answering an ad in The Wall Street Journal.

Today, he is on the leading edge of a generation that is facing a huge emotional and financial burden from a disease that leaves victims requiring full-time nursing care. He is urging a national mobilization against what he describes as a looming Alzheimer’s “epidemic.”
Mr. Essner often speaks publicly about the disease, stepping outside his role as corporate chief and into the public policy arena. Last month, he testified at a Senate hearing, recommending that the National Institutes of Health double its current annual funding of $643 million for Alzheimer’s research.

Seated recently at a conference table at the company’s headquarters on pastoral property near Madison, N.J., Mr. Essner said he has taken to the podium because he thinks Alzheimer’s should garner the same attention that AIDS received during the 1980s and 1990s, when a coalition of government and industry worked feverishly to find treatments.

He says he is concerned as much about the disease’s dehumanizing effects as he is about its costs. “You see mothers who don’t recognize their daughters,” he says.CLICK HERE FOR MORE

Home Visits by Researchers Would Boost Alzheimer's Trials
MONDAY, June 11 (HealthDay News) -- Home visits by researchers may help increase the number of caregivers who are willing to enroll Alzheimer's disease patients in clinical trials, a new study finds.

It could also boost the number of patients who stay enrolled in trials, the University of Pennsylvania researchers added.

The team interviewed 108 caregivers of Alzheimer's patients who lived in the community. Caregivers were asked about their willingness to enroll their loved ones in hypothetical studies which differed according to four variables: location of study; method of transportation to study visits; chance of receiving a drug or placebo; and level of risk of the study drug.

Of the 108 caregivers, 17 percent were willing to take part in a high-risk clinical trial with no amenities. That increased to 27 percent when home visits were added and to 60 percent when low risk, home visits, and a higher chance of the patient receiving an active treatment were included, the study found.

The option of having home visits (which eliminates the inconvenience of traveling to a clinic) offset the negative study features, such as taking a high-risk drug. It also made caregivers of sicker patients more willing to sign up for studies, the researchers said.

"Altering studies to include home visits could result in shorter recruitment periods and increased patient retention rates," study author Jason Karlawish, associate professor of medicine and associate director of the PENN Memory Center, said in a prepared statement.

"The amount of time we save through these alterations could offset the added costs of the home visits, and, in fact, we may save considerable time and expense if the participants don't have to come in to the clinic so often," he said.

The study was to be presented at the Alzheimer's Association International Conference on Prevention of Dementia, in Washington, D.C.

"Other than lack of sufficient funding, recruiting and retaining clinical volunteers is now the single greatest impediment to developing better treatment and prevention strategies for Alzheimer's," William Thies, vice president for medical and scientific relations at the Alzheimer's Association, noted in a prepared statement.

More information
The Fisher Center for Alzheimer's Research Foundation has more about taking part in a clinical trial.

Early Alzheimer's Detection by Gene 'Signature' In Blood Possible

Early Alzheimer's Detection

With anticipation running high of breakthroughs in Alzheimer's disease therapies, reports of the latest results from studies on early detection of Alzheimer's took on added urgency.

The studies included examination of blood samples examined for a "signature" set of genes, an innovative analysis of both MRI and PET scan images, novel combinations of memory and cognitive tests, and a predictive model based on an easy-to-assess mixture of test results and health/lifestyle history.

"Potential disease modifying drugs for Alzheimer's are very likely on the horizon, so we need accurate and easy-to-use early identification techniques for Alzheimer's so that we can initiate treatment earlier," said William Thies, PhD, vice president of Medical and Scientific Relations at the Alzheimer's Association. "And until disease modifying drugs are available, early detection empowers people to plan for their future sooner, including financial and legal matters, along with getting access to resources such as support groups, disease information and research studies."

Improvements in early detection of Alzheimer's in recent years have granted researchers and service providers, such as the Alzheimer's Association, access to a population of people who are able to articulate their experiences and needs.

"By better understanding the experiences of people living with Alzheimer's, we can significantly improve clinical studies, medical practice, caregiving and services," Thies said.

Still, a large proportion of people with Alzheimer's are not diagnosed until the disease is in the moderate or advanced stages, according to the Alzheimer's Association.

"The National Institute on Aging, the Alzheimer's Association and industry are pushing hard for earlier detection and earlier intervention through efforts such as the Alzheimer's Disease Neuroimaging Initiative (ADNI)," said session moderator and neuroimaging expert Michael Weiner, MD, of the San Francisco Veterans Affairs Medical Center and the University of California, San Francisco, who is ADNI's principal investigator. "Ultimately, we hope that brain and biological changes in Alzheimer's can be detected before memory decline and other symptoms appear."

Gene "Signature" In Blood May Detect Alzheimer's

At the Alzheimer's Association Prevention Conference, scientists working for Norwegian biotech company, DiaGenic ASA, presented results of a study using an assay that detects a unique gene expression profile or "signature" in blood samples.

Researchers combed through many Alzheimer patient samples and several thousand genes to identify what they believe to be a common gene signature for Alzheimer's that they could test. The most informative genes isolated in these discovery phase studies were then used to design and develop customized test arrays. The scientists presented results from a cohort of 119 subjects (53 with Alzheimer's, 58 age matched controls, and 8 younger controls), using two different detection technology platforms. The researchers generated one gene "signature" using about 1,200 genes giving a specificity of 84 percent, a sensitivity of 86 percent and thus an accuracy of 85 percent. A second "signature" within a 96-gene setting gave a specificity of 73 percent, a sensitivity of 84 percent and an accuracy of 79.5 percent.

"As with all new diagnostic tests, ours will also require validation with a large number of Alzheimer's patients and control subjects at multiple centers. This is already in progress, and next year we'll know how well the test will perform," said Anders Lonneborg, PhD, Research Director at DiaGenic ASA. [CLICK HERE FOR MORE...]

Nolan just wants dad to remember: Father of 49ers coach losing ground in battle with Alzheimer's disease
By Dennis Georgatos, MEDIANEWS STAFF

49ers head coach Mike Nolan is coping with a father who has Alzheimer's disease.

Nolan plans to phone his dad next Sunday and wish him the best on Father's Day, like he always does. But there's a difference this year.

"I don't know if he'll recognize me, but I'll call him still," the 49ers coach said.

Dick Nolan, the first half of the only father-son tandem to coach the same NFL team, is losing ground in his battle with Alzheimer's disease, with his recent failures to recognize even his closest family members the most telling and heartbreaking indicator.

The elder Nolan has struggled for several years with Alzheimer's. The disease attacks nerve cells in the brain, destroying memory and the ability to think clearly and perform daily tasks, from brushing teeth to remembering which key unlocks the front door.

Over the past year, Mike Nolan said, his father's condition has degenerated, compounded by a worsening case of prostate cancer.

"Last summer, the 49ers alumni here held a reunion for him, and that was great," Nolan said. "He was still able to communicate with all the guys and know who was who. But right now, he wouldn't know those same guys."It's been difficult. It has been most difficult for mom and for my three siblings who live in Dallas, because they're around Dad every day."

Nolan and his wife, Kathy, have traveled to Dallas twice in the past four months. On the most recent trip three weeks ago, Nolan, along with his six siblings, were with their mother, Ann, to help arrange their father's placement in a care facility for dementia and Alzheimer's patients.

The family's decision arose from the increasing difficulties Ann Nolan encountered in trying to take care of her 75-year-old husband at home.

"One of the things I thought was sad that happened was he didn't recognize my mother as his wife," Nolan said. "So when she tried to help him with anything from just showering or using the bathroom — he's a very modest man — he wouldn't let her even be in there, and he really wasn't able to get it done right. It became very difficult for her to help him."

Nolan has largely avoided speaking publicly about his father's illness for the past two years. Even when he was named 49ers coach Jan. 19, 2005, 37 years to the day after his father began coaching the team, Nolan decided against having him at his introductory news conference. The elder Nolan had begun showing signs of Alzheimer's, and his son wanted to spare him from a potentially uncomfortable public moment.

Mike Nolan also knew the elder Nolan often forgot he had been diagnosed with Alzheimer's. If he saw or heard anything in the paper or on TV linking him to the illness, it would be like finding out for the first time that he had it, and that potentially could happen over and over again. Each time, his father agonized over the ramifications of the illness and the realization, in his flickering awareness, that he could no longer help his son do his job.

Last week, though, Mike Nolan began speaking out in hopes of raising awareness of Alzheimer's and dementia. He also wanted to help get the word out about the "88 Plan," a joint program by the league and the players union to provide up to $88,000 a year to help pay for the care of former players with dementia or Alzheimer's.

The plan takes its name from the number worn by Hall of Fame tight end John Mackey, who has dementia.

While there is no known definitive link between multiple concussions and the onset of Alzheimer's or other dementia conditions, some studies indicate it could be a factor.
Dick Nolan, an "88 Plan" participant, played nine years in the NFL as a defensive back, and Mike Nolan said his dad "had a lot of concussions, as all of them did back then.

"I don't know" whether they were a factor, Nolan said. "I don't pretend to be a doctor or scientist. But I certainly appreciate what they're doing as far as research and as far as the medical plan the NFL is doing for them. And I want them to continue to do it so we can find a cure for this. A lot of people have it."

Through it all, Nolan said, he has come to understand what people mean when they say someone with Alzheimer's disease or dementia "dies twice."

"When they don't know who you are any longer, that's tough to deal with," he said.

With his father, it's not a total blackout — yet. Nolan said when he arrived in Dallas for his visit in late March, his father initially recognized him. But soon after, his father — the rough-and-tumble cornerback, the co-inventor with Tom Landry of the "flex defense" — seemed to be in a daze.

"Those momentary recognitions, when he'll reach out, when he'll say something, those are the hardest," Nolan said, his voice quieting to a whisper. "I mean, there's that ray of light, and then it's gone."

Alzheimer's Patients Get RFID Chip

(June 11, 2007) Twenty-five Alzheimer's patients were implanted with radio frequency identification chips that can be linked to their medical records. The patients were implanted last week at the 2007 Alzheimer's Educational Conference in West Palm Beach, Fla.

The chips, from VeriChip Corp., Delray Beach, Calif., work with the vendor's VeriMed Patient Identification System. Each chip contains a 16-digit identification number that is linked to a patient's medical records in a database at the medical facility. Waving the vendor's RFID reader over a patient implanted with a chip can capture the number. Emergency personnel can also use the scanner to identify patients.

The event was sponsored by Alzheimer's Community Care, a local provider organization. Those who elected to receive the chip are not part of VeriChip's recently announced study with the organization, which will implant 200 Alzheimer's patients and their caregivers with the chips. In the study, the patient's medical record will include their Alzheimer's diagnosis, related medications, caregiver contact information, and other information.

For more information, go to verichipcorp.com.

Alzheimer's Cases May Quadruple

(WASHINGTON) — More than 26 million people worldwide have Alzheimer's disease, and a new forecast says the number will quadruple by 2050. At that rate, one in 85 people will have the brain-destroying disease in 40 years, researchers from Johns Hopkins University conclude.

The new estimates, being presented Sunday at an Alzheimer's Association conference in Washington, are not very different from previous projections of the looming global dementia epidemic with the graying of the world's population.

But they serve as a sobering reminder of the toll to come if scientists cannot find better ways to battle Alzheimer's and protect aging brains.

"If we can make even modest advances in preventing Alzheimer's disease, or delay its progression, we could have a huge global public health impact," said Johns Hopkins public health specialist Ron Brookmeyer, who led the new study.

The biggest jump is projected for densely populated Asia, home of almost half of today's Alzheimer's cases, 12.6 million. By 2050, Asia will have 62.8 million of the world's 106 million Alzheimer's patients, the study projects.

A recent U.S. study estimated that this nation's Alzheimer's toll will reach 16 million by 2050, compared with more than 5 million today. The new estimate is significantly lower, suggesting only 3.1 million North American cases today and 8.8 million by 2050.

Among the estimates for other regions are:
*Africa, 1.3 million today and 6.3 million in 2050.
*Europe, 7.2 million and 16.5 million.
*Latin America and the Caribbean, 2 million and 10.8 million.
*Oceania, 200,00 and 800,000.

The project was funded by Elan Pharmaceuticals and Wyeth Pharmaceuticals.

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AAN: Second-hand Smoke Can Add to Dementia Risk - CME Teaching Brief® - MedPage Today

BOSTON, May 1 -- Long-term exposure to second-hand smoke may be a risk factor for dementia in the presence of subclinical carotid artery disease, said investigators here.In a subset of patients in the Cardiovascular Health Study, those who had a subclinical carotid stenosis and lived with a smoker for 30 years or more had a 2.5-fold greater risk for dementia than those free of cigarette smoke exposure, found statistician Thaddeus Haight, M.A., of the University of California at Berkeley.

This study was published as an abstract and presented orally at a conference. These data and conclusions should be considered to be preliminary as they have not yet been reviewed and published in a peer-reviewed publication.

In contrast, second-hand smoke exposure in the absence of carotid disease was not a significant risk factor for dementia, reported Haight at the American Academy of Neurology meeting.
The findings did not meet the test of statistical significance, but pointed to second-hand or passive smoking as a possible additive risk factor for dementia.

"It's actually quite plausible that second-hand smoke, given its effects on the cardiovascular system, can affect the risk of dementia indirectly through the clinical cardiovascular disease pathway," he said. "But what's less well known is whether there are actually direct effects that may be neurotoxic effects with respect to people's cerebral functioning, and the neurotoxic effects of second-hand smoke with respect to some neurodegenerative process."

It's also not known whether passive smoking has an effect on dementia through subclinical processes, he said. He and colleagues looked at cumulative exposure to second-hand smoke among 985 men and women who were never active smokers. There were 728 women and 257 men from the ages of 66 to 92 years, most of them in the 70- to 74-year age range.

The participants had no previous history of cardiovascular disease (myocardial infarction, angioplasty, angina pectoris, coronary artery bypass, claudication, stroke and/or transient ischemic attack), and had no prior diagnosis of dementia.

There were indications in some patients, however, of subclinical cerebrovascular disease, measured by initimal thickness of cerebral vessels on MRI, and on carotid ultrasound findings, Haight said.

Of these patients, 495 reported second-hand smoke exposure, defined as living fulltime with a smoker, for a mean 27.9 years, range one to 80 years. Some 50% of the patients had no second-hand smoke exposure, 25% had low exposure, defined as one to 30 years of living with a smoker, and 25% had high second-hand smoke exposure (more than 30 years cohabitation with a smoker).

The authors used marginal structural Cox proportional hazards models to calculate the causal relative hazard of clinical cardiovascular disease with respect to dementia over seven years.
They examined the effects within strata of age, age-adjusted SHS, and separately for cerebral vascular disease (infarct less than 3 mm, infarct 3 mm or greater, or white grade matter disease) and carotid artery disease (25% or greater stenosis, or more than 80 percentile common or internal wall thickness).

During the study, 10% of the patients developed clinical cardiovascular disease, and 15% developed dementia. "What we found was that second-hand smoke in and of itself did not independently contribute to incidence of dementia," Haight said. "But what we did see was that among those people with subclinical cardiovascular disease, based on carotid artery ultrasound, that there was in fact some suggestion of an interaction in the group with the highest levels of second-hand smoke exposure and abnormal carotid ultrasound findings, and incident dementia."

The relative hazard for dementia was 2.5 among those patients with subclinical cardiovascular disease and at least three decades of exposure to someone else's smoke, and 1.5 for those with cardiovascular risk factors but lower exposure (one to 30 years), compared with patients with no subclinical disease and no second-hand smoke exposure.

The associations between second hand smoke and dementia did not, however, meet the statistical significance level of P<0.05,>

ACC: Dark Chocolate Improves Vascular Function - CME Teaching Brief® - MedPage Today [CLICK HERE TO READ ARTICLE]

Wyo. seeing rise in Alzheimer's

CHEYENNE, Wyo. (AP) - Wyoming is predicted to see a 43-percent increase in Alzheimer's Disease this decade - among the highest increases in the nation, according to information a foundation released recently. The Alzheimer's Association predicts the Mountain West will be the epicenter of the nation's growth in the mind-destroying illness. Wyoming ranks fourth out of the 50 states in projected increases between 2000 and 2010, while Colorado and Alaska tied for first with projected 47-percent increases. Carol Monge, director of communications for the Colorado Chapter of the Alzheimer's Association, said the risk of Alzheimer's increases as people age. She said the West has attracted a lot of retirees and already had a lot of baby boomers.

"The greatest risk of Alzheimer's is when someone turns 65 or older," Monge said. "And when baby boomers age, that's going to cause a great increase." Beverly Morrow, administrator of the Aging Division at the Wyoming Department of Health, said the study's findings were no surprise. She said a study released early this year by the AARP predicted Wyoming will see a 114-percent increase in Alzheimer's by 2025, which would also put the state fourth in the nation.

"When you combine a very big baby boom generation that is aging with medical advances keeping people alive longer, we know that the proportion of Alzheimer's cases is going to continue rising," Morrow said. Morrow said Wyoming lacks a dedicated diagnostic center for Alzheimer's Disease.

"I think right now people are not getting diagnosed as early as they could and getting early intervention because we don't have a diagnostic center in Wyoming," she said.

Morrow said it will also be increasingly important for Wyoming to expand services to those who care for Alzheimer's patients. "If we can't get help to keep their loved one at home, and all those cases get dumped on the public system, we're just not going to be able to handle it," Morrow said.

Mary Hein, executive director of Alzheimer's Wyoming, said she believes the Alzheimer Association's report predicting increases in cases in the state is correct based on the number of calls her organization has been receiving and the amount of interest expressed at recent meetings. "The hard part is judging how it's happening, because in the very beginning stages, it's so difficult to diagnose, and people don't always go to a physician," Hein said.

Experts say that while nothing has been shown definitively to prevent Alzheimer's, they say staying active seems to reduce the risk. "What's good for the heart is good for the brain," Monge said, including exercising, eating well and keeping cholesterol and blood pressure under control.

"Take on a new hobby, do crossword puzzles, learn a foreign language," Monge said. She said that staying socially involved with friends and family also seems to help.

Cellzome Receives First Milestone Payment for Alzheimer's Program from Ortho-McNeil Pharmaceutical, Inc.

BOSTON, Massachusetts, March 13/PRNewswire/ -- Cellzome Inc. announced today that it has received the first milestone payment for its Gamma Secretase Modulator (GSM) program in connection with the selection of a lead compound by Ortho-McNeil Pharmaceutical, Inc. under its agreement with Cellzome. Ortho-McNeil entered into a collaboration and license agreement with Cellzome in May 2005 and the collaboration was extended for a further year in January 2007.

Tim Edwards, Cellzome's CEO, said: "I am delighted with the progress we have made in our collaboration. This milestone payment is a reflection of the continued productivity of Cellzome's drug discovery group in working with our collaborator to advance toward preclinical development a potential oral therapeutic for patients with Alzheimer's disease, and further demonstrates the utility of our leading chemical proteomics technology."

About Cellzome Inc.
Cellzome is a privately owned drug discovery company applying its world-class technology to the discovery of novel small molecule therapeutics. Cellzome is commercializing its assets and technology by developing its own pipeline of small molecule kinase inhibitors for inflammatory disease, and by collaborating with leading pharmaceutical companies.

Cellzome's emerging pipeline includes a small molecule Histamine H4 receptor antagonist, initially for asthma and allergic rhinitis, which is scheduled to begin clinical studies early 2008. In addition, Cellzome is applying its distinctive Kinobeads(TM) technology to the discovery and development of novel, selective, kinase inhibitors targeting key inflammatory mediators in immune receptor signaling and chemotaxis, including ITK, ZAP70and PI3Kgamma.

The Company also has a large non-exclusive research collaboration with Novartis Institutes for Biomedical Research Inc. (NIBRI), using Cellzome's leading proteomics capability to discover new drug targets and leads in a variety of disease areas; this was recently extended to June 2008.

Cellzome is intent on developing both organically and through merger or acquisition. Cellzome's holding company is domiciled in the USA and it employs about 80 people in total at its facilities in Cambridge, UK and Heidelberg, Germany. To learn more about Cellzome, please visit our website: www.cellzome.com

About Alzheimer's disease
Alzheimer's disease is an irreversible, progressive brain disease that slowly destroys memory and thinking skills. It is the most common cause of dementia in older people. About 20 million people are affected worldwide and at the current rate the number is expected to double by 2025. In the United States alone, more than 4.5 million people are currently afflicted with the disorder, resulting in healthcare costs of close to $ 100 billion annually. According to Cellzome estimates, this therapeutic market is currently valued at about $4.7 billion in the major markets (US, UK, Germany, France, Italy, Spain and Japan) and is expected to increase to $7.8 billion by the year 2010.

The first symptoms of Alzheimer's disease usually set in after the age of 60. With the degeneration of healthy brain tissue, intellectual and social abilities are lost and patients eventually are left with little comprehension or awareness.

Amyloid plaques are the pathological hallmark of Alzheimer's disease and form as the disease develops in the brains of Alzheimer's patients. Genetic studies in recent years have shown that the protein in these plaques, called amyloid-beta or simply Abeta, is a central part of the mechanism that causes the disease. Abeta peptide is generated from a large transmembrane precursor protein, called APP, by two subsequent proteolytic cleavages that occur close to, or within the membrane. The first cleavage is carried out by an aspartic protease called gamma-secretase (BACE) and the second cleavage is carried out by a multi-protein complex called gamma-secretase. Cellzome has mapped the protein interaction network around this process and identified several target candidates.

Medivation CEO to Present at Leerink Swann & Company's Roundtable Conference on Alzheimer's Disease

SAN FRANCISCO, March 27 /PRNewswire-FirstCall/ -- Medivation, Inc. (Nasdaq: MDVN) today announced that David Hung, M.D., president and chief executive officer, will participate in Leerink Swann & Company's Roundtable Conference entitled "A Mind Is a Terrible Thing to Waste: Emerging Treatments for Alzheimer's Disease," on Tuesday, April 3, at Le Parker Meridien in New York. Dr. Hung will present at 9:15 a.m. Eastern Time.

Dr. Hung will provide an overview of Medivation and its clinical development program for Dimebon(TM) for Alzheimer's disease.

Full top-line data from Medivation's Phase 2 efficacy study of Dimebon in Alzheimer's disease were presented at the 8th International Conference on Alzheimer's and Parkinson's Diseases: Progress and New Perspectives in Salzburg, Austria, on March 18. Six-month results from this randomized, double-blinded, placebo-controlled trial of Dimebon in patients with mild-to- moderate Alzheimer's disease demonstrated that patients treated with Dimebon were significantly improved compared to patients taking placebo on all five efficacy endpoints studied, which assessed cognitive function, memory, ability to perform tasks of daily living, global function and behavior. Dimebon was well tolerated in this study.

A live audio webcast of Dr. Hung's presentation will be available on the "Events and Presentations" page of the "Investor Relations" section of the Company's website at http://www.medivation.com. A replay will also be available for 30 days following the live presentation.

About Medivation
Medivation, Inc. is a biopharmaceutical company that acquires promising technologies in the late preclinical development phase and develops them quickly and cost-effectively. Medivation's current portfolio consists of small molecule drugs in development to treat three large, unmet medical needs -- Alzheimer's disease, Huntington's disease and hormone-refractory prostate cancer. The Company intends to build and maintain a portfolio of four to six development programs at all times. For more information, please go to http://www.medivation.com.

This press release contains forward-looking statements, which are made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. Forward-looking statements involve risks and uncertainties that could cause actual results to differ significantly from those projected. You are cautioned not to place undue reliance on the forward-looking statements, which speak only as of the date of this release. You are also cautioned that none of the Company's product candidates has been approved for sale, that significant additional animal and human testing is required in order to seek marketing approval for any of its product candidates, and that Medivation cannot assure you that marketing approval can be obtained for any of its product candidates. Medivation's filings with the Securities and Exchange Commission, including its Annual Report on Form 10-KSB for the year ended December 31, 2006, include more information about factors that could affect the Company's financial and operating results.

Multiple Studies Point to Deeper Connections between Diabetes and Alzheimer’s Disease

GEN News Highlights
There is a growing body of scientific evidence that links Alzheimer’s and diabetes, which may enable already approved diabetes therapies to be quickly tested for effectivene