Tuesday, April 22, 2008
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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?
We're using monthly pocket calendars, small enough to fit in a man's pocket or a woman's purse.
Each day on the calendar is divided into scheduled events, things to be done today but at no particular time, and then notes on anything — like the weather forecast or the fact that grapes are on sale at the supermarket. This type of memory training system has been successful with people who have had memory loss from brain injuries.
We're testing it with people who have mild cognitive impairment. While the physical causes of their memory problems are different, the practical outcome is the same. And the system seems to work for both.
What's the difference between mild cognitive impairment and Alzheimer's?
Mild cognitive impairment is a transition stage between the cognitive changes of normal aging and the more serious problems caused by Alzheimer's disease. It often includes the memory loss problems common to Alzheimer's, but doesn't meet the qualifications for full-blown dementia. While many people who have mild cognitive impairment go on to develop Alzheimer's, others don't. So a diagnosis of mild cognitive impairment doesn't necessarily mean you will certainly develop Alzheimer's. Because the cognitive problems are less severe in MCI, there is greater opportunity to use nonmemory skills to compensate for memory problems.
How do people with memory problems remember to use the calendar?
We work with them for six weeks, so that it becomes a habit. It's kind of like driving a stick shift or typing on a computer keyboard. You don't think about all the motions involved in the process. You don't say to yourself, "OK, now I'm going to depress the clutch with my left foot and move the shifter with my right hand." You just do it. One of our participants compared it to golfing. He doesn't think about how to position his head or his hips. He just does it. In addition to writing things in the calendar, we also ask our participants to look at their calendars at least twice a day. Three times is even better. At breakfast, they can look over what they're supposed to do that day. They need to check the day before, too, to see if there are any unfinished tasks that need to be carried forward. We also tell them to check things off right when they do it. So even if they don't remember doing something — if it's checked off, they must have done it.
Does just writing things down help people remember?
Writing it down helps it stick in your memory. Saying it out loud as you're writing it down also can help cement it in your memory. I tell people to use all their senses to help jog their memory. I had a big test to study for recently, and I said things out loud and had color-coded reminder notes. I even drew pictures. The good thing about this calendar is that it can encompass whatever works for you. This sounds helpful even for people who don't have memory loss problems. This can benefit all sorts of people. I personally never kept a calendar until this. I got a planner and followed right along with the study participants.
Lots of people need something like this.
For example, they'll get a phone call and then jot a phone number on the newspaper and then throw the paper away.
One of our participants came in with a big stack of Post-it notes and scraps of paper, all bound together with a rubber band. We've just translated that into one system, so people can find what they need easily when they need it.
Is it working for the people in your study?
Almost every person in the study has said that it has helped them. That has been very satisfying. Some people are still at it after more than a year. That's really something, to have people change the way they do things and have it stick. Every person who participates in this study is accompanied by a support person, usually a spouse or child. And these support people often say, "It's so nice not to have to answer the same question over and over."
Are there other benefits?
It helps make our participants feel a little bit more independent — that they don't have to rely on other people to remember things for them. This system also gives them a way of feeling they are doing something pro-active. Many people feel the control slipping out of their fingers. By giving them back some personal responsibility and control, it's really making a difference in that individual. It's hitting both needs at the same time.
How long does this technique hold off the types of memory lapses that lead to loss of independence?
We don't know yet. In my mind, it's a "use it or lose it" scenario. You need to keep your brain engaged in attending to these things, or they're gone.
This is basically a holding maneuver.
Some people may think they don't need it now, that they're functioning OK.
But it's like muscle memory. If they get it to become a habit, it will help them be prepared for that day when they really do need it.
Saturday, April 12, 2008
The Great Forgetting - New York Times
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
Friday, April 11, 2008
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.
CLICK HEADLINE TO VIEW FULL ARTICLE...
Wednesday, April 9, 2008
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 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.
CLICK BELOW FOR FULL STORY
Medical News: EB: OTC Painkillers Also Help Grandpa Get Buff - in Geriatrics, General Geriatrics from MedPage Today:
Tuesday, April 8, 2008
Alzheimer's Disease - Symptoms, Diagnosis, Treatment of Alzheimer's Disease - NY Times Health Information
NY Times Health
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 »
In the early stages, the symptoms of AD may be subtle and resemble signs that people mistakenly attribute to "natural aging." Symptoms often include:
Having trouble finding names for familiar objects
Getting lost on familiar routes
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:
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.
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.
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.
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.
In-Depth Report ...Alzheimer's Disease
Finding Alzheimer’s Before a Mind Fails- New York Times
"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
Researchers Find Huge Variations in End-of-Life Treatment - New York Times
FTD - Frontotemporal Dementia - Brain Disease - Pick's Disease - Creativity - 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
Monday, April 7, 2008
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