Friday, March 30, 2007
ACC: Dark Chocolate Improves Vascular Function - CME Teaching Brief® - MedPage Today [CLICK HERE TO READ ARTICLE]
Tuesday, March 27, 2007
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.
"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.
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'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
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.
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 effectiveness against the deadly brain disease. New data from drug trials and long-term population studies were presented at “ICAD” being held in Madrid, Spain. Weili Xu, M.D., and colleagues from the Karolinska Institute and the Stockholm Gerontology Center, Sweden, followed 1,173 individuals and found that borderline diabetes was associated with an almost 70% increased risk of developing dementia and Alzheimer’s disease in this population. Further analysis revealed that such a significant association was present only among non-carriers of APOE e4 allele, a gene that increases the risk for the most common form of Alzheimer’s. The risk for Alzheimer’s was especially high when borderline diabetes occurred with severe systolic hypertension. Another study by Rachel A, Whitmer, Ph.D., of Kaiser Permanente’s division of research, and colleagues suggests that people with type 2 diabetes have an increased risk of dementia and Alzheimer’s disease and among those, the patients with poor blood sugar control are at the greatest risk. Dr. Whitmer studied 22,852 patients with type 2 diabetes for eight years and compared the levels of glycosylated hemoglobin with the risk for dementia. They found that in patients with elevated glycosylated hemoglobin levels the risk for dementia increased and those with levels above 15% had an 83% higher risk. A third study, presented by Donald R. Miller, Sc.D., from the Boston University School of Public Health and the Center for Health Quality, Outcomes, and Economic Research, and colleagues found that patients treated with thioazolidinediones, such as pioglitazone (Actos) or rosiglitazone (Avandia), were 20% less likely to develop Alzheimer’s disease than those on insulin.
Scientific Founder of TorreyPines Therapeutics Honored by Alzheimer's Association: [PR Newswire]
Second Gene Associated with Late-Onset Alzheimer’s Discovered
GEN News Highlights
A team of researchers have uncovered the second gene for late-onset Alzheimer’s disease. Since the 1993 discovery of APOE, this latest gene, SORL1, was seen to be replicated in four distinct ethnic groups. The team believes that the reduction of SORL1 in the brain increases the likelihood of developing Alzheimer disease.
The team of scientists was led by Robert Friedland, M.D., professor in the department of neurology at Case School of Medicine in collaboration with an international effort led by Boston University School of Medicine (BUSM), the University of Toronto, and Columbia University Medical Center.
"Understanding how the forms of the SORL1 gene associated with increase risk alters protein handling will suggest novel pharmacological or lifestyle modifications to slow progression," predicts Dr. Friedland.
In a paper published in the February issue of Nature Genetics, researchers describe how variants in the SORL1 gene were found to be more common in people with late-onset Alzheimer's than in healthy people of the same age. The team suggests that these genetic variations alter the normal function of SORL1, resulting in Alzheimer’s disease. People with these genetic variants may not produce normal amounts of SORL1, implying that this gene has a protective function when working properly.
Another aspect of their findings was that the association between Alzheimer’s disease and SORL1 was replicated in four distinct ethnic groups: North American and European caucasians, African-Americans, Caribbean-Hispanics, and Arabs residing in Israel. Previous studies on the genetics of Alzheimer's used data from mostly Caucasian populations of American and European ancestry. This five-year study involved DNA samples from 6,000 volunteers.
Newswise: Who Gets Heart Failure? Race Takes Back Seat to Diabetes and High Blood Pressure
Newswise — Diabetes and high blood pressure, two conditions rooted in genetics and environmental surroundings, play a much greater role than race alone in determining who is mostly likely to develop heart failure, according to the latest study from cardiologists at Johns Hopkins. Each year, nearly 300,000 Americans die from heart failure.
Experts say that racial disparities have long been known to exist in who actually develops risk factors for the condition, with African Americans nearly twice as likely to be diagnosed with diabetes and more than a third as likely to have high blood pressure than Caucasian Americans. But researchers have only now determined the precise role played by race in comparison to other risk factors, including socio-economic factors, age, gender, smoking, family history, and other health problems, as well as diabetes and hypertension.
The Hopkins team will present its findings March 27 in New Orleans at the American College of Cardiology’s annual Scientific Sessions in New Orleans.
In the study, researchers monitored nearly 7,000 men and women, age 45 to 84, of different ethnic backgrounds and with no existing symptoms of heart disease. African Americans developed heart failure at significantly higher rates (4.6 cases per 1,000 per year) than all other races, including Hispanics and Caucasians. Their rate was almost five times that of Chinese Americans (1 case per 1,000 per year) and almost twice that of Caucasians (2.4 cases per 1,000 per year).
However, these apparent risk differences among races almost disappeared (dropping from twice as likely, a significant difference, to no more than one-and-a-half times as likely, an insignificant difference) when researchers used statistical techniques to exclude the two traditional risk factors for heart disease.
“When all major factors are taken into account, the differences between races for heart failure largely evaporate in the absence of diabetes and hypertension among African Americans,” says senior study investigator João Lima, M.D.
According to Lima, an associate professor of medicine and radiology at The Johns Hopkins University School of Medicine and its Heart Institute, these early results add to other interesting findings from the so-called Multiethnic Study of Atherosclerosis (MESA).
The study, started in 2001, is monitoring its ethnically diverse participants for six to eight years to see who develops heart failure and who does not. It is the first large-scale analysis of racial or ethnic differences in heart function. So far, 79 study participants have developed congestive heart failure.
Other results presented at the meeting showed differences among races in heart strain, or contraction, which may contribute to disparities in heart failure, albeit to a lesser extent. Indeed, African American hearts were found to contract less strongly than those of Hispanic, Caucasian or Chinese American backgrounds.
Lima cautions, however, that much remains to be understood about the root causes of racial disparities and how to fix them.
He points out that while African Americans are at much higher risk of heart failure, there is no similarly higher number for risk of suffering heart attack, which, like diabetes and hypertension, often leads to heart failure.
In MESA, researchers found a reverse relationship, with African Americans having the lowest rates of heart failure due to myocardial infarct (at 25 percent), while other races had a much higher proportion: Caucasians (40 percent), Hispanics (42 percent), and Chinese Americans (100 percent.)
Lima says the difference could be due to successful disease prevention efforts among all racial groups, except for African Americans, at controlling hypertension.
“A lot of public health attention has already been paid to getting high blood pressure under control, so it may be just that this risk factor is under tighter control in some ethnic groups than in others,” he says. “African Americans are clearly getting heart failure from causes other than heart attack.”
According to lead researcher Hossein Bahrami, M.D., M.P.H., the message to physicians is clear, “warding off heart failure in African Americans requires aggressive treatment of diabetes and hypertension. Whether through increased screening or greater emphasis on drug therapies, these are two risk factors that must be brought under control.”
Bahrami, a senior cardiology research fellow at Hopkins, says removing barriers for African Americans to controlling their diabetes and hypertension could be critical to reducing new cases of heart failure. Across all ethnic groups, an estimated 550,000 Americans are diagnosed each year.
Bahrami says the team’s next steps are to determine why different rates exist for these risk factors and the role played by biological and environmental factors. Funding for this study, which is taking place in six centers in the United States, comes from the National Heart, Lung and Blood Institute, a member of the National Institutes of Health.
Besides Lima and Bahrami, another Hopkins investigator involved in this study was David Bluemke, M.D., Ph.D. Study co-authors were Richard Kronmal, Ph.D., from the University of Washington in Seattle; Kiang Liu, Ph.D., from Northwestern University in Chicago, and Gregory L. Burke, M.D., M.S., from Wake Forest University in Winston-Salem, N.C.
Fend off heart disease with fish.
The Greenland Inuit eat an incredibly high-fat diet with few vegetables, yet their rate of heart disease is stunningly low. Chalk it up to all the fatty fish they eat: The staple food in their diet is fish rich in omega-3 fatty acids. You've probably heard by now that omega-3s fend off heart disease -- something that could be right around the corner if your blood sugar is stuck in overdrive. It's no wonder fish makes our list of Magic foods.
A study at the Harvard School of Public Health found that women with diabetes who ate fish just once a week had a 40 percent lower risk of dying from heart disease than did women with diabetes who ate fish less than once a month.
But omega-3s do more than protect your heart. They also quell inflammation in the body, a major contributor to numerous chronic diseases of aging, including insulin resistance and diabetes. It may even play a role in brain diseases such as Alzheimer's as well as certain cancers.
Of course, fish is also a protein food, and protein foods have virtually no impact on blood sugar. We suggest that you aim to eat fish for dinner once or twice a week when you might otherwise have chicken or beef. Make it baked, broiled, pan-fried, stewed, or grilled. Just don't make it fast food or deep fried, like fish and chips or a fish sandwich. Loaded with bad-for-you fats, this fare just isn't the same kettle of fish. One study found eating fried fish and fish sandwiches offered no heart benefits at all.
All fish contain some omega-3s, but fatty types such as albacore tuna, salmon, mackerel, lake trout, herring, and sardines are richest in them.
While the strongest proof of the health benefits of fish points to the heart, there's also plenty of research showing that food with fins can cut the risk of prostate cancer and help maintain brain power as you age. There's also evidence that fatty fish may help defend against depression.
SEATTLE, March 22 -- For depressed patients on medication but too sad to seek psychotherapy as well, lasting help may be available by phone researchers found in a follow-up study.
For more than 75% of nearly 400 patients, the positive effects of six months of brief telephone psychotherapy at the start of antidepressant medication endured for 18 months after the first session, including six months beyond the end of all phone therapy, said Evette Ludman, Ph.D., of the Group Health Cooperative Center for Health Studies here, and colleagues.
This study, reported by Dr. Ludman and colleagues in the April issue of the Journal of Consulting and Clinical Psychology, was a follow-up to a 2004 report on the same sample of 393 patients, published in the Journal of the American Medical Association.
The follow-up found that at 18 months, 77% of those given phone-based therapy reported that depression was "much" or "very much" improved, compared with only 63% of those receiving usual care.
In the 18-month analysis, the benefits of telephone psychotherapy in the first six months were sustained during the second six months when only brief booster sessions were provided. Significantly a "robust clinical benefit" endured for six months after all treatment contact was discontinued, the researchers found.
"As with weight control," Dr. Ludman said, "maintaining improvement is the hardest part of treating depression."
Traditional in-person psychotherapy has limited reach among the large number of patients beginning antidepressant treatment in primary care, the researchers wrote. Expanding access to therapy calls for considering new therapy approaches, such as phone-based sessions, that place greater emphasis on accessibility, outreach, and patient convenience, the investigators concluded.
Of the participants, 195 were randomly assigned to antidepressant medication and usual care while 198 got medication and phone therapy. Of these, 348 (89%) completed the six-month blinded assessment, and 334 (85%) completed the 18-month follow-up.
On average, all patients reported a moderate level of depressive symptoms at baseline, two to four weeks after starting antidepressants prescribed by a primary-care provider.
Phone psychotherapy sessions, delivered by masters-level therapists, included eight core sessions (about 30 minutes) during the first six months, with 15- to 20-minute booster sessions every two months up to a year. After that, phone therapy ended.
According to a structured cognitive behavioral-based psychotherapy program, patients were encouraged to identify and counter their negative thoughts (cognitive behavioral therapy), pursue activities they had enjoyed in the past, and develop a plan to care for themselves....[MORE]
Wednesday, March 21, 2007
Alzheimer's Growth Shows Need for Increased FDA Funding
WASHINGTON, March 21 /PRNewswire-USNewswire
A new estimate by the Alzheimer's Association shows that more than five million Americans are living with Alzheimer's disease -- a 10 percent growth over previous estimates and a number that could more than triple in the coming decades unless new treatments and cures are developed for the debilitating illness.
The new numbers re-emphasize the need for a strong and adequately funded drug safety review program at the Food and Drug Administration to ensure that new Alzheimer's disease drugs can be safely and rapidly brought to market, according to the Coalition for a Stronger FDA.
"As the population ages, more and more American families will be touched by Alzheimer's disease," said Tommy G. Thompson, co-chairman of the Coalition and the former Secretary of the Department of Health and Human Services. "We simply can't afford for the FDA to be a bottleneck for new drugs and treatments because it is not adequately funded."
The Alzheimer's Association estimates that without a cure or effective treatments to delay the onset or progression of Alzheimer's disease, the prevalence could soar to 7.7 million people with the disease by 2030 and 16 million by the middle of the century. More information on the Alzheimer's Association report can be found at http://www.alz.org/news_and_events_rates_rise.asp.
"The funds needed by the FDA will be repaid hundreds of times over in health care savings by getting new Alzheimer's disease drugs quickly and safely to market," said Stephen McConnell of the Alzheimer's Association, a member of the Coalition. "It's an investment we can't afford not to make."
"We are committed to delivering transformational therapies to Alzheimer's patients within the next decade," said Daniel Perry of Accelerate Cure- Treatment for Alzheimer's disease, a member of the Coalition. "A lack of sufficient FDA appropriations stands in the way of delivering treatments that could lessen the human and economic tolls that Alzheimer's exacts on patients and their loved ones."
The Coalition for a Stronger FDA -- a diverse group of consumer, non- profit, patient and industry groups -- is committed to working with Congress and the administration to give the FDA the resources it needs to fulfill its mission. As part of a five-year process to significantly expand the agency's budget, the Coalition is seeking $175 million in increases for 2008 over the fiscal year 2007 budget, including $40 million for drug review programs, $115 million for food safety programs and $20 million for medical device programs.
The increases will allow the FDA to build confidence in the public health system, speed innovation in medical technology, ensure the United States remains competitive in foreign markets, and boosts public confidence in the agency and its mission.
Specifically, a $40 million increase in the drug budget in 2008 would allow the FDA to provide faster and safer approval of products that are saving lives and transforming health care; promote new drug technologies that will revolutionize pharmaceutical therapies and ensure continued U.S. leadership in drug innovation; enhance the surveillance capability over new drugs once they reach the market; and further integrate emerging science into the regulatory process.
About the Coalition
The Coalition for a Stronger FDA is designed to be a multi-year effort with the following goals: (1) making sure the FDA has sufficient resources to protect patients and consumers and (2) maintaining public confidence and trust in the FDA. Tommy G. Thompson, Donna E. Shalala and Dr. Louis Sullivan -- the last three Secretaries of the Department of Health and Human Services -- are the co-chairs of the Coalition. Member organizations of the Coalition include patient groups, consumer advocates, public health organizations and innovative companies. A list of members and more information on the Coalition can be found at http://www.fdacoalition.org.
By JANE GROSS
More than five million Americans have Alzheimer’s disease, a 10 percent increase from the last official tally five years ago, and a number expected to more than triple by 2050, absent a cure, as the 85-and-over population soars and the baby boomers move into their late 60s and 70s.
Much of the report is a synthesis of existing research on the prevalence and costs of the disease. But the report includes the startling finding that 200,000 to 500,000 people younger than 65 have some form of early onset form of dementia, including a rare form of Alzheimer’s disease that strikes people in their 30s and 40s.
Mary Mittelman, an Alzheimer’s researcher at New York University, had mixed feelings about disproportionate attention to early onset Alzheimer’s disease. On the one hand, Dr. Mittelman said, these cases are such a small minority that she fears will take focus and resources “from the majority who are much older.” On the other, she said, "because of the ageism of this society” far too many people still believe dementia to be part of normal aging and attention to this younger group will clarify that it is a "real disease.”
Apart from early onset cases, the primary risk factor for Alzheimer’s disease is age.
Alzheimer’s disease, the most common form of dementia, affects memory, reasoning and communication. In the advanced stage, people need help dressing, using the bathroom and eating. In the final stages, they cannot speak or recognize family members. The disease is ultimately fatal.
Currently, there are five drugs approved by the Food and Drug Administration that slow the disease’s symptoms for 6 to 12 months in half the individuals who take them. Nine other drugs are in late-stage trials.
Yesterday’s report was released at a hearing in Washington, where Congress is considering a bipartisan bill to increase research money.
The report itemizes the cost to the federal government in Medicare spending. Care for a patient with dementia costs three times as much as care for the average beneficiary — $13,207 a year vs. $2,454 — and overall dementia-related Medicare costs are expected to more than double, to $189 billion, by 2015.
Other costs include the value of unpaid care provided by family and friends to the vast majority of Alzheimer’s patients who live at home.
Estimates were based on research by the Rush Alzheimer’s Disease Center in Chicago, which analyzed incidence of the disease locally. That incidence information was then extrapolated to national prevalence using census population figures and census projections.
Thursday, March 15, 2007
BOSTON, March 14 -- Supplemental beta carotene over 12 years had no beneficial effect on the occurrence rate of age-related maculopathy, found researchers here.
This finding emerged from the Physicians' Health Study 1, a randomized, double-blind, placebo-controlled trial with 22,071 U.S. male physicians, ages 40 to 84, reported William Christen, Sc.D., of Harvard's Brigham and Women's Hospital, and colleagues, in the March issue of the Archives of Ophthalmology.
The study had tested beta carotene and low-dose aspirin in this group, and found no benefit and no harm after 12 years' use of beta carotene on cancer or cardiovascular disease as the end points, Dr. Christen said.
The current age-related maculopathy study used the randomized beta carotene component of the study. Participants were randomly assigned to receive 50 mg of beta carotene every other day or placebo. Maculopathy was defined as a reduction in best-corrected vision to 20/30 or worse....[MORE]
CME Teaching Brief® - MedPage Today - Strokes Stop Essential Brain Crosstalk
ST. LOUIS, March 14 -- Spatial neglect -- a common attention-deficit sequel to stroke -- appears to be caused by a lack of communication between two regions of the brain, according to researchers here.
The finding contradicts the traditional explanation that spatial neglect is caused by damage to a specific brain region, said Maurizio Corbetta, M.D., of Washington University.
Instead, magnetic resonance imaging showed that patients with neglect -- in which patients have difficulty paying attention to one side of their bodies or the visual field -- have disrupted connections between dorsal and ventral frontoparietal attention networks, reported Dr. Corbetta and colleagues in the March 15 issue of Neuron.
"For more than a century, we have linked neurological deficits and their recovery to the damage done to neurons directly affected by a stroke or other injury," Dr. Corbetta said in a statement. ...[MORE]
CME Teaching Brief® - MedPage Today - FDA Warns of Sedative-Aided Sleep Driving and Anaphylaxis
ROCKVILLE, Md., March 14 -- The FDA has taken steps to ensure that clinicians and patients are aware of rare bizarre effects associated with sedative hypnotics, including driving or eating while sleeping.
The agency has ordered makers of all sedative-hypnotic drugs to strengthen label warnings about the risk of "complex sleep-related behaviors" and also severe allergic reactions. The FDA defined sleep driving as "driving while not fully awake after ingestion of a sedative-hypnotic product, with no memory of the event."
Last December, the FDA sent letters to manufacturers of products approved for the treatment of sleep disorders requesting that the whole class of drugs revise product labeling to include warnings about the following potential adverse events:
Anaphylaxis and severe facial angioedema, which can occur the first time the product is taken. Complex sleep-related behaviors which may include sleep-driving, making phone calls, and preparing and eating food while asleep.
"There are a number of prescription sleep aids available that are well-tolerated and effective for many people," said Steven Galson, M.D., MPH, director of FDA's Center for Drug Evaluation and Research. "However, after reviewing the available post-marketing adverse event information for these products, the FDA concluded that labeling changes are necessary to inform health care providers and consumers about risks."
Russell Katz, M.D., director of the FDA's division of neurology products at the center, said the new label will warn that a number of complex-sleep related behaviors "including cooking and eating, using the telephone, having sex, and driving" have been reported by persons using the drugs. Typically, the patient has no memory of these actions.
At a press briefing today, Dr. Katz repeatedly emphasized that the allergic reactions, including anaphylaxis and angioedema, and the complex sleep-related behaviors,"are rare by any definition" and he said the FDA has not received any reports of death associated with either side effect....[MORE]
Newswise - When Your Brain Talks, Your Muscles Don't Always Listen
Newswise — Have your neurons been shouting at your muscles again? It happens, you know.
As we grow older, neurons--the nerve cells that deliver commands from our brains--have to “speak” more loudly to get the attention of our muscles to move, according to University of Delaware researcher Christopher Knight, an assistant professor in UD's College of Health Sciences.
“As a result of age-related changes in muscle and neurons, elderly people are often frustrated by poor control during precision tasks, and slowed physical responses contribute to more falls as people grow older,” Knight said.
Knight and co-author Gary Kamen, who directs the Exercise Neuroscience Laboratory at the University of Massachusetts, recently published the results of a study on motor-unit firing rates in the Journal of Applied Physiology, and Knight is now beginning a new project focusing on motor-control mechanisms in the elderly. Both studies are sponsored by the National Institutes of Health.
The ultimate goal of the research, Knight said, is to improve movement quality in older adults, as well as patients with disorders such as cerebral palsy or multiple sclerosis, or who are recovering from strokes.
Every move you make is made possible through a miraculous communications network involving the brain at the command center, the spinal cord, billions upon billions of nerve cells, and thousands of muscle fibers.
“Muscles are the driving force behind our movements,” Knight said. “Every time they get a command from the neurons, the muscle fibers contract. In the generation of muscular force, the smallest controllable unit consists of an individual neuron and the muscle fibers it stimulates. We believe that our research is very important to our understanding of motor-control mechanisms in general and impaired control in patient populations.”
Shedding light on the communication between neurons and muscles, and how it changes as we age, may lie right at our fingertips, according to Knight's research.
Using an experimental apparatus he and his students created in UD's Human Performance Lab, Knight has been examining muscular force on a very small scale in the index finger, specifically, the first dorsal interosseous muscle. Located between the index finger and the thumb, this muscle contains 120 “motor units”--in other words, 120 individual neurons, or nerve cells, and the muscle fibers they activate.
“It's a relatively simple muscle, so you get to see more of a one-to-one relationship between the activity of the neurons and the resulting muscular force,” Knight said....[MORE]
Tuesday, March 13, 2007
BOSTON, March 12 -- Beta-amyloid plaques in the brains of people with Alzheimer's type dementia can be spotted with the aid of the imaging agent Pittsburgh Compound B, researchers here determined.The distribution of amyloid plaques seen on positron emission tomography imaging with the tracer compound closely correlated with that discovered post-mortem in a 76-year-old man with Lewy body dementia, reported Brian J. Bacskai, Ph.D., of Massachusetts General Hospital and the University of Pittsburgh, and colleagues.
"What it says is that if you see positive Pittsburgh Compound B, you're going to find that that person has amyloid pathology in their brain, and that's a valuable first step," said co-author Steven T. DeKosky, M.D., director of the Alzheimer's Disease Research Center at the University of Pittsburgh, in an interview.
Commenting in an accompanying editorial, David M. Holtzman, M.D., of Washington University in St. Louis, agreed.
"This is an important case report, as for the first time it documents correspondence between cortical Pittsburgh Compound B retention and amyloid deposition in a human," Dr. Holtzman wrote.
"The advent of in vivo amyloid imaging has led to great hope that this type of technique will aid in the differential diagnosis of dementia, serve as an antecedent biomarker for Alzheimer's disease, and be useful in determining whether agents designed to clear amyloid are effective. This article provides strong validation that Pittsburgh Compound B retention is very likely reflective of beta-amyloid that is deposited as amyloid."...[MORE]
Tuesday, March 6, 2007
Alzheimer's rewrites ending of this love story
Connie Lesko calls the relationship between her mom and dad a wonderful love story.
Paul and Eloise Bledsoe met as teens in their native West Virginia, growing up during the Great Depression and treasuring all they had, including each other. Paul always showed affection toward his wife, kissing her, hugging her, pinching her. Eloise always playfully resisted.
Connie is one of their four children, and they gathered wonderful memories as Paul sought a better life for his family. They first moved to Ohio and then to Fort Myers, where he worked as a welder.
Today, those memories are more difficult to grasp. <more>
Decreased Brain Density
Older adults who complain their “mind is going” may be losing a part of their brain along with their memory, according to a recent study (Neurology, Sept. 12, 2006).
The study, which looked at 120 people over the age of 60, found people who complained of significant memory problems but still had normal performance on memory tests had reduced gray matter density in their brains even though they weren’t diagnosed with Alzheimer’s disease or mild cognitive impairment (MCI), which is a transition stage between normal aging and the more serious problems caused by Alzheimer’s disease.
When compared to healthy individuals, the study found people who complained of significant memory problems had a 3 percent reduction in gray matter density in an area known to be important for memory; there was a 4 percent reduction among individuals diagnosed with MCI.
“Significant memory loss complaints may indicate a very early ‘pre-MCI’ stage of dementia for some people. This is important since early detection will be critical as new disease modifying medications are developed in an effort to slow and ultimately prevent Alzheimer’s disease,” said study author Andrew Saykin, PsyD, professor of psychiatry and radiology at Dartmouth Medical School in Lebanon, New Hampshire.
While normal aging, MCI and Alzheimer’s disease have been associated with the loss of gray matter in the brain, this is believed to be the first study to quantitatively examine the severity of cognitive complaints in older adults and directly assess the relationship to gray matter loss.
Dr. Saykin said the findings highlight the importance of cognitive complaints in older adults, and suggested that those who complain of significant memory problems should be evaluated and closely monitored over time. Memory complaints, a cardinal feature of MCI which confers high risk for Alzheimer’s disease, are reported in 25 to 50 percent of the older adult population.
The study was supported by the National Institute on Aging, the Alzheimer’s Association, the Hitchcock Foundation, the Ira DeCamp Foundation, the National Science Foundation, New Hampshire Hospital and the National Alliance for Medical Image Computing.
Thursday, March 1, 2007
Sarasota's Roskamp Institute Discovers New Class of Drugs That Can Impact Alzheimer's Disease
The Roskamp Institute announced today the discovery of a new class of drugs that lower the production of the main pathological protein that causes Alzheimer's disease. The discovery is detailed in an article co-authored by Drs. Daniel Paris and Michael Mullan and currently appears in Neuroscience Letters.
The Roskamp Institute, which is devoted to finding treatments for Alzheimer's disease, has been researching drugs that have the potential to stop the production of B-amyloid.
NF-kB (a protein that occurs in all cells in the body) activity results in inflammatory responses due to the switching on of genes that encode proteins that are key in inflammation. NF-kB inhibitors are being developed widely in the pharmaceutical industry primarily for its use in inflammatory conditions such as Arthritis and, until now, have not been thought of as a potential treatment for Alzheimer's.
At the same time, many drug companies are searching for compounds that can lower or stop the production of B-amyloid. The finding that NF-kB controls B- amyloid production means that NF-kB inhibitors might be developed as anti- Alzheimer drugs. One such example is Celastrol, which is researched in the Roskamp Institute's publication, and is available as a food supplement but has never been formally tested in Alzheimer's.
"Although we have known about the important inflammatory role of NF-kB for a long time, we did not know that it controls B-amyloid production," said Dr. Daniel Paris, Senior Scientist of the Roskamp Institute. "This may be one way that the inflammation caused by B-amyloid leads to more B-amyloid being produced -- a positive feedback loop with awful consequences for the sufferer."
The publication details the NF-kB findings and explains why this family of drugs should be tested for their use in treating Alzheimer's disease patients.
For more information on the Roskamp Institute and to view the journal article in Neuroscience Letters, please visit us online at http://www.RoskampInstitute.com.
The article can also be viewed directly at http://www.roskampinstitute.com/pdf/NF_kB_Publication.pdf.