Alzheimer's Pathology Related To Episodic Memory In Those Without Dementia
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Alzheimer's pathology can appear in the brains of older men and women without dementia or mild cognitive impairment. The pathology is related to loss of episodic memory, according to a new study published in the June 27, 2006, issue of Neurology, the scientific journal of the American Academy of Neurology.
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The study evaluated 134 older men and women who didn't have cognitive impairment at the time of their death. Participants came from the Religious Orders Study and the Memory and Aging Project. Both are longitudinal, clinical-pathologic studies of older persons without dementia who underwent annual clinical evaluations and several cognitive performance tests. After they died, their brains were examined at autopsy for evidence of pathology.
More than a third of the participants (50) met criteria for a pathologic diagnosis of Alzheimer's disease. Criteria included lesions of brain tissue on the autopsy. This group also scored significantly lower than the other participants on tests for episodic memory, such as recalling stories and word lists.
"The results provide evidence in support of the idea that some type of neural reserve can allow a large number of older persons to tolerate a significant amount of Alzheimer's pathology without manifesting obvious dementia," said study author David A. Bennett, MD, of the Rush Alzheimer's Disease Center in Chicago.
Scores on the Mini Mental State Examination, a mental status screening test of cognitive functions, were nearly identical for participants with and without a pathologic diagnosis of Alzheimer's disease.
"This study questions the acceptability of minor episodic memory loss in older adults as 'normal'," said Carol F. Lippa, MD, who wrote an editorial in the same issue of Neurology. "Maybe this early decline in episodic memory precedes mild cognitive impairment and should be the target of research efforts in the early detection of Alzheimer's disease."

Older people at higher risk of dementia do not benefit from a combination of vitamin B and folate, say researchers from the University of Otabo, Dunedin, New Zealand. Even after two years of taking the vitamins daily, volunteers did not better in cognitive tests than those who were given a placebo. Click link to read more.
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Memory Loss In People With Diabetics
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Researchers at the University of Edinburgh are aiming to pinpoint why diabetes can cause memory loss and mental decline. A thousand people will take part in the study, the largest of its kind ever undertaken in the UK. The research team will ask people with Type 2 diabetes - associated with an increased risk of memory impairment and dementia - aged 60-75 years to complete puzzle-based tests and have their heart function and blood sugar levels measured. Follow up tests four years later will find out if there have been any changes in brain function. Dr Mark Strachan, an honorary senior lecturer at the University and a consultant in diabetes and endocrinology at the Western General Hospital, said: "People with type 2 diabetes are at increased risk of developing problems with memory and problem-solving abilities. Although the cause of these abnormalities is not understood, various risk factors associated with diabetes may be important. For example, in some cases, high blood sugar levels can be damaging to small blood vessels in the eyes, nerves and kidneys and there is evidence that the same damage - microvascular disease - can occur in the brains of people with diabetes. "The main aim of this study is to find out which risk factors, including microvascular disease, inflammation and alterations in hormone levels are linked to altered brain function in people with diabetes. This information is crucial in determining the cause of diabetes-related memory problems and other changes in brain function such as problem-solving abilities and attention span." He added: "Diabetes affects around three per cent of the UK population, and about 170,000 people in Scotland are known to be affected. The prevalence of diabetes is increasing but we are better at treating its complications, such as heart disease. As a result, people with diabetes are likely to live longer and so cognitive problems are likely to become a much bigger issue."

Alzheimer's pathology can appear in the brains of older men and women without dementia or mild cognitive impairment. The pathology is related to loss of episodic memory, according to a new study published in the June 27, 2006, issue of Neurology, the scientific journal of the American Academy of Neurology. Click link to read more.
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Curing Alzheimer's
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America is getting serious about preparing for the possibility of an outbreak of avian flu. Would that it could muster the same sense of urgency for a disease that is already here and is certain to become epidemic. The disease is Alzheimer's. It will claim one in 10 baby boomers, create a personal and fiscal nightmare for their families, and drain -- if not bankrupt -- state and federal health-care budgets. Medicare now pays one-third of all its health-care funds for some 4.5 million Alzheimer's patients. Are we ready for three times that number?
Alzheimer's doesn't have to be an inevitable part of aging. It is a disease for which research can find a cure, or at least a more effective treatment. The FDA now needs to give the same priority status to drugs for Alzheimer's as it has for AIDS and cancer treatments. And, the federal government needs to designate Alzheimer's as a No. 1 research priority.
If we don't do these things, the projections are staggering. Within the next five years, nearly a half-million new Alzheimer's cases will be diagnosed annually, as 78 million baby boomers reach age 65. Given those numbers, most of us will either become an Alzheimer's patient, care for one in our home or know a patient in our extended family. By robbing victims of memory, Alzheimer's strips away individuality, dignity and independence.
Alzheimer's is expensive. It requires $19,000 a year in out-of-pocket costs for each caregiver family. Last year Medicare spent $91 billion for Alzheimer's. That figure will nearly double in just four years -- and keep soaring as 14 million cases are diagnosed in boomers' lifetimes.
Within the pharmaceutical industry, there are 28 Alzheimer's compounds in development. But progress on all fronts is unconscionably slow considering the looming shadow of this epidemic. And, given the complexity of the disease, no single research organization has the resources to research all its facets as quickly as we must.
At Wyeth alone, we've committed hundreds of millions of dollars to this research. We are moving in a promising direction by testing eight innovative approaches. Right now no one can say that any one of them will work. But we believe that, through taking multiple "shots on goal" in our research labs, a treatment can be found.
In October 2001 Wyeth started its Alzheimer's research program with a vaccine approach designed to stimulate the body to stop the buildup of beta-amyloid plaque in the brain -- thought to be a critical part of the disease process. While that initial effort proved unsuccessful, it did not deter us from moving ahead with another vaccine approach. This new vaccine program is in the clinic. Furthest along in development at Wyeth is a pill -- a potent serotonin receptor antagonist that may enhance cognition in moderate cases and significantly enhance the quality of life. Another promising approach is an antibody directed against beta-amyloid. By removing these plaques, we hope to stop the disease from progressing.
But it is imperative for industry, scientists and regulators to work together to help us reach our goal even faster. We need a sense of urgency, a commitment to collaboration that will lead to a concerted, focused effort to prevent this impending epidemic.
A TV journalist who cares for a husband diagnosed with the disease wrote in a recent issue of the scientific journal Alzheimer's & Dementia: "Right now the majority of Alzheimer's victims and their caregivers are our parents. Their plight is our future. . . . We are desperately in need of access to new therapies instead of being left with only agonizing decisions."
For every month we hesitate, we will find ourselves spending down the nation's health-care budget to care for the demise of millions of people. We should be preparing to cure them. We could make my generation the last to dread Alzheimer's. It is time to accelerate the pace of our efforts and take the battle to a level on par with our hope.
By Robert Essner, president and chief executive of Wyeth Corp.

Alzheimer's more common than previously thought
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The number of Americans with Alzheimer's disease is probably two to three times more than current estimates, according to a new study. And as the population ages, Alzheimer's could become the most expensive disease in the country.
In the new study, brain autopsies of elderly people who had had no symptoms of Alzheimer's showed that more than a third had lesions in their brains that met the criteria for the disease. The cost of caring for people with the brain disease tops $100 billion a year, according to the Lasker Foundation.
In the study at Rush University Medical Center in Chicago, the scientists performed autopsies on the brains of 134 people who had scored normally on a battery of memory and behavior tests. Of the 134 people, 50 showed lesions typical of Alzheimer's disease but had not had memory problems that indicated they had the disease.
The people with Alzheimer's pathology did have minor, but significant, lapses in certain memory tests, Bennett found. As a group, those people scored about a quarter point lower than people without Alzheimer's plaques. But the difference is not enough to make individual diagnoses. The people with undiagnosed lesions were also older on average (86 years old) when they died than the people who didn't meet the standard for the disease (81.7 years old).
That could mean that given a few more years of life, the people who didn't have the lesions might have developed them. None of the brains was completely free of changes, Bennett said.
"It's hard to find a brain without any pathology in it," he said.
The researchers at Rush are studying more than 2,000 older adults without dementia. The volunteers came from two study groups: Catholic nuns, priests and brothers participated in the Religious Orders Study, while the Rush Memory and Aging Project drew volunteers from the community around the university. They agreed to donate their brains to the research.
Elsewhere, researchers are among those hoping to find solutions for the memory-robbing disease.
The risk of developing Alzheimer's doubles every five years after age 65. Almost 40 percent of people over age 85 have the disease. But older people shouldn't panic if an acquaintance's name slips their minds or they have other common lapses.
"As long as people are able to carry out their normal daily activities, they shouldn't worry if they occasionally misplace their eyeglasses or car keys," Morris said. "If they put their keys in the freezer and can't find them then, well, that's a change (in behavior), and they should be evaluated."
The new study raises the possibility that people who have plaques in their brains but who haven't experienced a drop in their mental capacity, may have some protective factors that keep them from getting dementia.
Most treatments are based on reducing the amount of damage the disease causes in the brain, Bennett said. "But we're saying, let the pathology accumulate. Let's just adapt brains to handle it better," he said. Studies have previously shown that mental and physical exercise and social networking are helpful in reducing risk of the disease.
Waiting to start treatment until someone develops dementia is probably too late, Morris said. He called for new methods to detect brain lesions before people's memories lapse, and for treatments to stop the progression of the disease. Researchers are testing almost a dozen drugs against Alzheimer's in clinical trials.
About 99 percent of people who develop Alzheimer's have sporadic cases. That means they do not have specific mutations or known genetic factors that cause the disease. The problem could be that as people age, they make too much amyloid-beta, or that the ability to clear it from the brain slows down. The excess protein - as much as 1,000 times more than normal levels - could then congeal into plaques.
But no one has been able to measure the cycling of the protein in people's brains before. The test involves infusing a compound to label the newly produced amyloid-beta, and then sampling cerebral spinal fluid over 36 hours in the hospital.
The researchers have factored in hidden Alzheimer's disease and expect that up to a third of their seemingly healthy controls could have altered amyloid-beta metabolism, he said.

Production of key Alzheimer's protein monitored for first time in humans
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Researchers from Washington University have developed the first safe and sensitive way to monitor the production and clearance rates of amyloid beta peptide (Abeta) in the human central nervous system, opening a valuable window into the genesis of Alzheimer's disease.
The scientists report on Sunday on the online issue of journal Nature Medicine that via an intravenous drip, they give test subjects a form of the amino acid leucine that has been very slightly altered to label it. And they can monitor the production and clearance rate of Abeta through the labeled leucine.
High levels of Abeta in the brain are a hallmark of Alzheimer's disease and believed to be a pivotal cause of the condition. Tests that measure Abeta levels in the cerebrospinal fluid have been available for some time. However, those fixed assessments of Abeta gave no indication of whether the flood of Abeta in patient's brains came from an increase in the mechanisms that make the protein or a reduction in the processes that regularly clear it from the brain.
Because Alzheimer's symptoms take many years to develop, some researchers had assumed that the creation and clearance rates for Abeta were very slow. But the initial test of the new technique, applied to six healthy volunteers, suggests the opposite.
"Abeta has the second-fastest production rate of any protein whose production rate has been measured so far," says lead author Randall Bateman, assistant professor of neurology.
Ideally, the production and clearance rates stay balanced, causing the overall amount of Abeta in the central nervous system to remain constant. Researchers are now applying the technique to individuals with Alzheimer's disease.
Researchers are developing Alzheimer's drugs that either decrease Abeta production or increase its clearance, Bateman notes, and the new test could be very important in determining which approach is most effective.
The test also may be useful in diagnosis of Alzheimer's prior to the onset of clinical symptoms, which occurs after Alzheimer's has inflicted widespread and largely irreversible damage to the brain.

Researchers in the University of Toronto's Department of Nutritional Sciences have some reassurance for diabetics and carb-counters. The glycemic index (GI), the table that lists the quality of carbohydrates in more than 750 common foods, works just as predictably whether subjects consume a single portion of one item, or a normal meal. Click link to read more.
http://www.medicalnewstoday.com/medicalnews.php?newsid=45862&nfid=al

New Clues To Biochemistry Of 'Anti-Aging'
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Published in the June 19-23 issue of Proceedings of the National Academy of Sciences, the study is the first to show that sirtuins directly control specific metabolic enzymes - called AceCSs - in mammalian cells.
The finding, which shines a spotlight on enzymes only recently thought to play a role in the biochemistry of "anti-aging," has attracted the interest of biotechnology companies seeking to make drugs that delay the aging process and age-related diseases. The drugs could target the metabolic enzymes to produce health benefits.
"Sirtuins are very enticing because of their ability to slow the aging process," says John Denu, associate professor of biomolecular chemistry at the UW-Madison School of Medicine and Public Health (SMPH) and lead author on the study. "They also have great potential for promoting healthier aging by giving us a better understanding of - and possibly suggesting treatments for - metabolic diseases such as diabetes and neurological disorders such Alzheimer's and Huntington's diseases."
Scientists studying the genetics and physiology of sirtuins in organisms such as yeast, worms, flies and mice have shown that this enzyme family plays a role in a variety of cellular processes, including gene silencing, cell death, fatty acid metabolism, neuronal protection and life span extension.
"In humans, sirtuins have been implicated in the health benefits of calorie restriction, which is known to lengthen life span, and the enzymes are activated when they are exposed to resveratrol, a plant product found in red wine also known to extend life span," Denu says. "In addition, elevated levels of sirtuins somehow slow degeneration in nerve cells that have been damaged, and the enzymes affect aspects of metabolism responsible for controlling insulin secretion."
Denu and his team, which has published widely on sirtuins, conducted test tube studies using mouse cells to learn exactly which molecular players sirtuins act on directly. Previous studies suggested that sirtuins control genes indirectly in the cell nucleus. The first hint that sirtuins might directly control metabolic pathways came from earlier work in bacteria done by UW-Madison bacteriology professor Jorge Escalante.

Could a Low-Carb Diet Slow Alzheimer's?
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A low-calorie diet, particularly one that's low in carbohydrates, may reduce or even reverse the symptoms of Alzheimer's disease, a new study in mice suggests.

Researchers at Mount Sinai School of Medicine in New York City report that restricting carbs may help prevent Alzheimer's by boosting brain activity associated with increased longevity.

"Both clinical and epidemiological evidence suggests that modification of lifestyle factors such as nutrition may prove crucial to Alzheimer's disease management," study author Dr. Giulio Maria Pasinetti, director of the Neuroinflammation Research Center at Mount Sinai, said in a prepared statement.

"This research, however, is the first to show a connection between Alzheimer's disease neuropathy by defining mechanistic pathways in the brain and scrutinizing biochemical functions," he said. "We hope these findings further unlock the mystery of Alzheimer's and bring hope to the millions of Americans suffering from this disease."

Alzheimer's disease is characterized by the buildup of plaque in the brain, caused by increased amounts of beta-amyloid peptides. These peptides stimulate a protein, called SIRT1, which affects aging.

In their study, the New York team studied mice fed a low-calorie, low-carbohydrate diet to see how it impacted the presence of beta-amyloid peptides in the brain.

The results, which appear in the July issue of the Journal of Biological Chemistry, showed that the restricted diet did, in fact, reduce peptides in the brain, while a diet high in saturated fat appeared to cause higher concentrations of peptides.

Leptin affects both appetite and memory
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The hormone leptin, which is secreted by fat cells and tells us when to stop eating, also affects long-term memory and learning.
In a report released this week, researchers at the Saint Louis University School of Medicine said they were studying the connection between obesity, Type 2 diabetes, and long-term memory loss, and decided to explore the role of leptin in these processes.
"In obese people, [leptin] doesn't cross into the brain to help regulate appetite," the research team said. "We've now found leptin affects the brain in other ways, compromising learning and memory. Low levels of leptin also could be related to cognitive deficits in disorders like Type 2 diabetes."
The scientists evaluated how well mice navigated a maze, then gave some of them leptin and sent all of the animals through the maze a second time.
The mice that got the leptin navigated the maze better than those that did not receive the hormone. Older mice with amyloid-beta plaques in their brain, typical of Alzheimer's disease in humans, responded the best, and showed benefit at a lower dose than younger mice.

Nature Medicine Publication Reports Positive Preclinical Data with ...DG News - USA... The findings in the Nature Medicine publication show that oral treatment of AZD-103 (scyllo-cyclohexanehexol) reduces accumulation of amyloid beta and amyloid ...

New vaccines may cure Alzheimer's diseasePeople's Daily Online - Beijing,China... The new vaccine targets genes responsible for the overproduction of amyloid-beta peptides, small ... of these plaques is the root cause of Alzheimer's disease. ...

Walking May Ward Off Alzheimer's
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The health benefits of regular walking may include helping prevent mental decline and Alzheimer's disease, research in patients aged 70 and up has found, bolstering evidence that exercise needn't be strenuous to be good for you.

There's plenty of evidence that mental exercise, such as crossword puzzles and reading, may reduce Alzheimer's risks, but previous studies on brain benefits from physical exercise had conflicting results.

The new findings, contained in two studies, clarify how much exercise might be beneficial and are good news for older people who want to avoid mental decline but "don't like doing all that awful, sweaty stuff," said Bill Thies, vice president for medical and scientific affairs of the Alzheimer's Association.

"This just says, `Go for a walk'" and bolsters evidence that what's good for the heart may be good for the brain, said Thies, who was not involved in the research.

"Keep eating your veggies, too" could be another mantra, according to a Dutch study, showing that Europeans ages 70 to 90 who ate a Mediterranean-style diet rich in fruits, vegetables, fish and olive oil had a 23 percent lower risk of death during a 10-year follow-up than those with less healthy eating habits.

A 65 percent lower mortality risk was found in those who combined the Mediterranean-style diet with three other healthy habits _ moderate alcohol use, no smoking and a half hour or more per day of physical activity, including walking.

The studies appear in Wednesday's Journal of the American Medical Association.

"This study is important because it is often thought that diet, alcohol, physical activity and smoking doesn't matter anymore in old age," said nutrition researcher Kim Knoops of The Netherlands' Wageningen University, who led the diet study.

While the studies involved older patients, they don't answer whether adopting healthy habits late in life has the same benefits as a lifetime of healthy behavior, since participants weren't asked how long they'd engaged in the activities.

One of the exercise studies involved 2,257 retired men in Hawaii ages 71 to 93. Those who walked less than a quarter-mile a day were almost twice as likely to develop Alzheimer's or other forms of dementia as men who walked more than two miles daily.

Walking was "probably representative of a lifetime behavior" for most of the men, given Hawaii's exercise-friendly climate, said University of Virginia biotstatistician Robert Abbott, the lead author.

A similar study, involving 16,466 female nurses ages 70 to 81, found that even women who walked a leisurely 1 1/2 hours a week did better on tests of mental function than less active women.

"We were a bit surprised that something so modest as walking would be associated with apparent cognitive benefits," said study author Jennifer Weuve, a Harvard School of Public Health researcher.

Thies offered some possible theories for how exercise might boost brain function.

He said research in mice has suggested that exercise might reduce brain levels of amyloid, a sticky protein that clogs the brain in Alzheimer's patients. Also, Thies said, studies have shown that exercise boosts levels of hormones necessary for nerve cell production, and increases blood flow to the brain.

A low-carb diet may help stave Alzheimer's
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NEW YORK, June 14 (UPI) -- New York researchers suggest that dietary regimens such as a low-carbohydrate diet might calm or even reverse symptoms of Alzheimer's Disease.
The study, published in the July issue of the Journal of Biological Chemistry, used an experimental mouse model to demonstrate that beta-amyloid peptides in the brain can be reduced by subjecting the mice to dietary caloric restriction, primarily based on low-carbohydrate food. Conversely, a high-caloric intake based on saturated fat was shown to increase levels of beta-amyloid peptides.
"Both clinical and epidemiological evidence suggests that modification of lifestyle factors such as nutrition may prove crucial to Alzheimer's disease management," says lead author Dr. Giulio Maria Pasinetti, director of the Neuroinflammation Research Center at Mount Sinai School of Medicine and lead author of the study.
"This research, however, is the first to show a connection between nutrition and Alzheimer's disease neuropathy by defining mechanistic pathways in the brain and scrutinizing biochemical functions."

New drug offers hope against Alzheimer'sToronto Star - Ontario, CanadaWhen the drug was given to mice that had been genetically altered to have Alzheimer's, it prevented the buildup of amyloid beta peptide, which causes the ...

A link between obesity and memory? Saint Louis University research ...EurekAlert (press release) - Washington,DC,USA... Mice with elevated levels of amyloid-beta protein, the brain plaques believed to cause Alzheimer's disease, and impaired learning and memory were "super ...

High Mental Activity Protects Against Alzheimer's
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Researchers at the Byrd Alzheimer's Research Institute in Tampa, Florida have determined that Alzheimer's mice placed in a mentally enriched environment outperform similar mice in traditional environments and behaviorally match those not suffering from the disease. The research, if extended to people with the disease, demonstrates that living a life full of mentally challenging activities can slow and even protect against the development of Alzheimer's disease. "What we are seeing in this research is that mice having the same characteristics as humans with Alzheimer's are able to perform well, even at the same level as mice without Alzheimer's, if housed in a mentally challenging, cognitively enriched environment. The mental stimulation provided in this environment appears to stymie mental impairment. After months of mental stimulation, it was impossible to differentiate these mice from the behaviorally normal, healthy mice," said Huntington Potter, Ph.D., investigator on the project and chief executive officer of the Byrd Research Institute. Potter said this successful Alzheimer's mouse experiment will be tested in Alzheimer's patients and that sessions of mentally stimulating activities would be given on a regular basis. It is hoped that such cognitive stimulation will stabilize or even improve the memory function of Alzheimer's patients. "If individuals with Alzheimer's can benefit from living in a cognitively enriched environment, then these individuals could live fuller, longer and more productive lives," said Potter. A high level of mental activity throughout life has been suggested to lower the risk of Alzheimer's disease, but it is impossible to assess the preventative potential of environmental enrichment in a controlled clinical study. The research done at the Byrd Alzheimer's Institute tackled this question by using Alzheimer's mice in a well-controlled, blind study. The experiments showed that the Alzheimer's mice living in the enriched environment outperformed those in standard housing when tested at an older age. The treated mice also were behaviorally indistinguishable from the mice without the Alzheimer's disease. The Byrd Alzheimer's Research Institute is based at the University of South Florida in Tampa. The National Institutes of Health recently designated the Byrd Alzheimer's Institute and USF as Florida's Alzheimer's Disease Research Center. Information on the study can be found at: http://www.byrdinstitute.org/ .

Transcription Factor Protein's Role In Cell Death, Neurodegeneration And Schizophrenia...

Gene based vaccine for Alzheimer's
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Researchers and scientists in Japan say that they have created the world's first gene-based vaccine for Alzheimer's. Research performed on lab mice, proved very encouraging as all of the mice that were given the gene based drug responded very well.
The vaccine works by attacking the genes that are responsible for the production of amyloid-beta peptides, which are little proteins that can form plaques in the brain leading to the emergence of Alzheimer's.
Dr. Yoh Matsumoto, who led the research states, that the vaccine is better than drugs that are used in treating the disease, due to the fact that harmful side effects are not a bi-product of using the drug, and plans to continue testing the drug on monkeys. .
"DNA vaccines are given by intramuscular injection, which stimulates the production of anti-amyloid-beta antibodies," Matsumoto said. The drug allows for the person's or in this case, the mice immune system to recognize these dangerous plaques and fend them off at a much higher rate than has been seen previously.

A Sweet Solution for Alzheimer's Disease?AScribe - USA... some types of a sugar called cyclohexanehexol - also known as inositol - prevented the accumulation of amyloid beta deposits, a hallmark of Alzheimer's disease ...

Transition Therapeutics Alzheimer's Disease Drug Candidate AZD-1036
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Nature Medicine Publication Reports Positive Preclinical Data With Transition Therapeutics Inc. ("Transition") announced that Nature Medicine, one of the world's leading peer reviewed medical journals, has published an online version of a publication of preclinical studies with Transition's lead Alzheimer's disease drug candidate, AZD-103. The AZD-103 compound is a possible disease-modifying therapeutic drug candidate for the treatment of Alzheimer's disease. This unique class of drug candidates may provide significant advantages over the current therapies on the market. The findings in the Nature Medicine publication show that oral treatment of AZD-103 (scyllo-cyclohexanehexol) reduces accumulation of amyloid beta and amyloid beta plaques in the brain, as well as reduces or eliminates learning deficits in a transgenic mouse model of Alzheimer's disease. Transition is pursuing the clinical drug development of AZD-103 in an expedited manner and today, also announced that dosing with AZD- 103 has commenced in Phase I clinical trials.
"Publication in the prestigious journal Nature Medicine of this pioneering work from leading researchers at University of Toronto provides very strong scientific validation for the potential efficacy of AZD-103 as an Alzheimer's therapeutic. We recognize the tremendous need for effective Alzheimer's therapies and are taking all steps to accelerate the advancement of AZD-103 into Phase II clinical trials in Alzheimer's patients later this year or early 2007", said Dr. Tony Cruz, Chairman and Chief Executive Officer of Transition.
The publication entitled "Cyclohexanehexol inhibitors of A Beta aggregation prevent and reverse Alzheimer phenotype in a mouse model," is accessible online in an electronic version at (http://www.nature.com/nm/journal/vaop/ncurrent/index.html) and will be available in a future issue of Nature Medicine (Citable publication number doi:10.1038/nm1423). The publication was authored by world-renowned Alzheimer's researchers at the University of Toronto using a widely-accepted transgenic mouse model of Alzheimer's disease.

Recommendations for Therapeutics and Prevention
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Dementia and age-related macular degeneration (AMD) are major causes of disability in the elderly. n–3 Fatty acids, particularly docosahexaenoic acid (DHA), are highly concentrated in brain and retinal tissue and may prevent or delay the progression of dementia and AMD. Low dietary intakes and plasma concentrations have been reported to be associated with dementia, cognitive decline, and AMD risk. The major dietary sources of DHA are fish and fish oils, although dietary supplements are available. At this point, it is not possible to make firm recommendations regarding n–3 fatty acids and the prevention of dementia and AMD. Our own unpublished observations from the Framingham Heart Study suggest that 180 mg/d of dietary DHA (2.7 fish servings/wk) is associated with an 50% reduction in dementia risk. At least this amount of DHA is generally found in one commercially available 1-g fish oil capsule given daily. n–3 Fatty Acids: Recommendations for Therapeutics and Prevention

International News Service - Sydney,Australia... Scientists suspect a rather active protein known as beta amyloid promotes the development of Alzheimer's disease, John Hardy, chief of the NIA's neurogenics ...Progress Being Made Toward Alzheimer's Cure: Clock is Ticking for ...

BioWorld Online - Atlanta,GA,USA... the neurotransmitter acetylcholine in the brain and other tissues of the body, whereas A beta 42 is a peptide involved in creating the amyloid plaques found in ...Axonyx, TorreyPines Merger Done For CNS Drugs, Listing

Drink Coffee
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Next time you have a deal to clinch or a colleague to win over, do it over coffee.
But make sure your arguments are sound as your audience is paying attention and will be quick to weed out weak points, says Queensland University of Technology researcher Dr Blake McKimmie, one of a team of psychologists who studied the effects of caffeine on cognition and persuasion.
The team found a moderate amount of caffeine could influence persuasiveness of an argument because it increased a person's attentiveness and allowed them to scrutinise a message more closely. "If you have drunk a moderate amount of caffeine - about two cups of coffee for a 60kg person - you are better able to evaluate an argument and if that argument is strong then you could be more likely to be persuaded," Dr McKimmie said. But, he says, with caffeine there is a fine balance between being alert and able to concentrate and being "wired".
"Research suggests if you have too much caffeine you are likely to be unable to pay as much attention to the actual message but be distracted by peripheral things such as the attractiveness of the person serving the coffee."
The research team asked people about their attitudes to voluntary euthanasia and abortion before they had drunk orange juice containing caffeine. They also questioned another group who were given plain juice. Each group was given a persuasive argument on the topics to read after the drink. "We found a marked increase in attention to the messages and the amount of positive message-related thoughts in the group who had had the caffeine," Dr McKimmie said.
"These differences were related to increased persuasion by the strong message for those people who consumed the caffeine." He said the finding of increased recall in the people who had had a moderate amount of caffeine suggested "caffeine-content drinks on campus may not be not such a detrimental thing if used in moderation". But he cautioned that other research suggested caffeine influenced mood and physiological arousal which could have a negative impact on information processing. "This is because people in a positive mood tend to engage in less effort when thinking about things. "Increased concentration and better recall was found only after a moderate intake of caffeine. Too much caffeine and these effects may well be lost," he said.
The experiments were conducted in the morning, a time when caffeine is traditionally used to counteract the fatigue effects of the circadian rhythms, he said

Unraveling Alzheimer’s: Parallel Clues May Be Found Visualizing Plaques In Human Brain, Mad Cow–Type Diseases...

Axonyx and TorreyPines Therapeutics Announce Merger Agreement ...

Brain On Chip
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For the first time, scientists at the Max-Planck Institute for Biochemistry in Martinsried near Munich coupled living brain tissue to a chip equivalent to the chips that run computers. The researchers under Peter Fromherz have reported this news in the online edition of the Journal of Neurophysiology (May 10, 2006).
Before informational input perceived by the mammalian brain is stored in the long-term memory, it is temporarily memorised in the hippocampus*. Understanding the function of the hippocampus as an important player in the memory process is a major topic of current brain research. Thin slices of this brain region provide the appropriate material to study the intact neural network of the hippocampus.
Methods commonly used in neurophysiology are invasive, restricted to a small number of cells or suffer from low spatial resolution. The scientists in Martinsried developed a revolutionary noninvasive technique that enables them to record neural communication between thousands of nerve cells in the tissue of a brain slice with high spatial resolution. This technique involves culturing razor-thin slices of the hippocampus region on semiconductor chips. These chips were developed in collaboration with Infineon Technologies AG and excel in their density of sensory transistors: 16384 transistors on an area of one square millimeter record the neural activity in the brain.
Recording the activity patterns of the united cell structure of an intact mammalian brain tissue represents a significant technological breakthrough. Employing the new technique, the biophysicists working under the direction of Peter Fromherz were able to visualize the influence of pharmaceutical compounds on the neural network. This makes the “brain-chip” from Martinsried a novel test system for brain and drug research.
As early as 1991, Peter Fromherz and his co-workers succeeded in interfacing single leech nerve cells with semiconductor chips. Subsequent research gave rise to bidirectional communication between chip and small networks of a few molluscan nerve cells. In this project, it was possible to detect the signalling between cells via their synapses. The chips used in these studies were developed and produced by the scientists themselves. The production requirements of the chip described above made collaboration with industry indispensable. With the resulting novel hybrid system of neural tissue and semiconductor, the scientists take a great step forward towards neurochip prosthetics and neurocomputation.

Scientist: Experiment points to treatment of Alzheimer'sPress-Enterprise (subscription) - Riverside,CA,USA... In his experiment, Ethell injected the tails of Alzheimer's mice with beta-amyloid responsive immune cells from healthy mice. Those ...\

New medicines in Alzheimer's fight
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University of Washington scientists have begun testing two new drugs they hope will ease the symptoms and possibly prolong the useful lives of Alzheimer's disease patients, a group that is destined to grow by multitudes in the decades to come. Researchers hope the drugs, which take a new approach to the disease, will do a better job than the current generation of medications that slow progression for only a few years. "Right now in Alzheimer's disease, these [two new] drugs are the great hope," said Dr. Elaine Peskind, associate director of the UW Alzheimer's Disease Research Center at the VA Puget Sound Health Care System in Seattle. One of the new medications seeks to remove the brain-altering plaque that partially causes Alzheimer's; the other is designed to prevent its production, Peskind said. UW testing new medicines in Alzheimer's fight

A Gardenia fruit extract traditionally used in Chinese medicine to treat the symptoms of type 2 diabetes does indeed contain a chemical that reverses some of the pancreatic dysfunctions that underlie the disease, researchers report in the June 7, 2006, Cell Metabolism. Click link to read more. http://www.medicalnewstoday.com/medicalnews.php?newsid=44667&nfid=al
The Hordaland Homocysteine Study: A Community-Based Study of ...International News Service - Sydney,Australia... outcome in patients with homocystinuria due to cystathionine beta-synthase deficiency ... repair in hippocampal neurons and sensitize them to amyloid toxicity in ...
Researchers target Alzheimer’s gene vaccineArizona State University - Tempe,USAA hallmark of Alzheimer's disease is the accumulation in the brain of the protein amyloid-beta 42. Scientists at the Biodesign Institute ...

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By using positron emission tomography (PET) with the radiotracer 18F-FDDNP, UCLA scientists were able to detect increases in the brain pathology (of beta-amyloid plaques and neurofibrillary tangles) associated with the progression of Alzheimer's disease. Their results were presented during SNM's 53rd Annual Meeting June 3-7 in San Diego. "We have demonstrated that the worsening of memory and other cognitive functions is correlated with the increase of 18F-FDDNP brain binding in a progressive pattern closely matching the known pattern of pathology progression," explained Vladimir Kepe, assistant researcher at the David Geffen School of Medicine at the University of California, Los Angeles. "Our method is sensitive to detect the regional increases in pathology (or the nature of the disease) as well as spreading of pathology within the brain of the same person as the disease worsens over time," added the co-author of "Detection of MCI-AD and Control-MCI Conversions in Alzheimer's Disease Patients With [F-18]FDDNP PET." Alzheimer's is the most common form of dementia among older people; it is a progressive, irreversible brain disorder with no known cause or cure. More than 4.5 million Americans suffer from Alzheimer's and its symptoms of memory loss, confusion, impaired judgment, personality changes, disorientation and loss of language skills. Alzheimer's disease is marked by progressive deterioration of memory and other cognitive functions (attention, language, reasoning, etc.) due to the cell loss in the vulnerable neuronal populations, which form brain circuitry responsible for these cognitive functions, said Kepe. In clinical settings, Alzheimer's disease is diagnosed based on performance in a variety of tests examining memory loss, language skills and other cognitive functions, but these tests offer only diagnosis of probable Alzheimer's disease, he said. For a definite diagnosis, a brain autopsy is necessary to detect the presence of brain lesions: neurofibrillary tangles and beta-amyloid plaques. For nearly a decade, UCLA researchers under the leadership of Jorge R. Barrio and Gary W. Small have been investigating techniques to detect and measure the levels of both types of lesions in the brains of living Alzheimer's patients using PET and the radiotracer 18F-FDDNP, a molecular imaging probe that binds to the neurofibrillary tangles and beta-amyloid plaques. "18F-FDDNP was the first molecular imaging probe successfully used for imaging of neuropathological lesions in Alzheimer's disease patients with PET," noted Kepe. Combined with the results of PET studies using FDG, a radiotracer commonly used to measure decrease in brain metabolic activity caused by Alzheimer's, it provides valuable information about disease status. With 18F-FDDNP PET, scientists "can detect the presence of these lesions in different brain regions and measure their relative regional density," he said. "Because the lesions appear first in the medial temporal lobe and then slowly spread to the rest of the brain as the disease progresses, we can detect the extent of this spread and use 18F-FDDNP as an indicator of the disease progression," added the UCLA researcher. "This study brings us one step closer to using 18F-FDDNP PET in the clinical setting for the diagnosis of Alzheimer's," said Kepe, continuing, "The fact that the method can detect changes in pathology caused by the disease progression is very significant, it demonstrates the method's sensitivity."

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Dramatic improvment when given immune cells
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Researchers at the University of California Riverside (UCR) and the University of South Florida have found evidence that weakened or suppressed immune responses may be responsible for Alzheimer’s disease and that boosting the immune system of Alzheimer’s mice with cells from normal mice causes dramatic improvement in learning and memory. The findings, by Professor Douglas Ethell, assistant professor in the Biomedical Sciences Division of UCR in collaboration with Professor Gary Arendash of the Johnnie B. Byrd Institute and University of South Florida, were released this week by the prestigious journal Neurobiology of Disease. This new research is based on a 2002 report by Professor Ethell that found that beta-amyloid, a protein, increases the amount of the immune suppressor, Fas ligand, and that prolonged suppression of immune responses to that protein is implicated in Alzheimer’s disease. Ethell wondered if boosting immune responses to beta-amyloid could improve learning and memory in mice that develop Alzheimer’s. He teamed up with Arendash who had previously shown that vaccinating mice with beta-amyloid caused temporary improvements in Alzheimer’s mice. However, clinical trials with beta-amyloid vaccinations had been halted due to brain inflammation in some patients. In this study, however, Ethell and Arendash tried a different approach. They injected the Alzheimer’s mice with just the immune cells from normal mice that had been vaccinated with beta-amyloid. The researchers found that with just one injection the mice did significantly better on memory tests and that the improvements lasted one to two months after receiving the cells, which was the longest time-point they tested. Findings from this study may shift the search for an Alzheimer’s cure away from beta-amyloid injections. Instead, the research suggests that a subtle shift in immune responses to the protein may be all that is required for the development of an effective therapy for Alzheimer’s. “We believe these findings show that resetting the responsiveness of specific immune cells to beta-amyloid can provide an effective therapeutic approach to treating Alzheimer’s disease,” Ethell said. “Translating this research into the clinic may involve isolating immune cells from a compatible donor, expanding them in the lab and delivering them to an Alzheimer’s patient. As we learn more about these cells, it may be possible to isolate them from the Alzheimer patient’s own blood, reactivate them in the lab and then return those cells to the patient.”

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This New Masters Seminar Series will bring the recognized leadersin the various areas of Anti-Aging specialties together with A4Mmembers for 1-2 day intensive training Seminars prior to eachupcoming international congress. For more information, visit www.worldhealth.net/event

People living in small communities around the country will soon be able to find out if their community qualifies for government assistance to upgrade their drinking-water supply. Click link to read more.
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Lead Poisoning Is a Concern for a Healthy Memory
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Eighteen years later, people who worked in factories using lead have lesions in the “white matter” parts of their brains, according to a new study published in the May 23, 2006, issue of Neurology, the scientific journal of the American Academy of Neurology. The white matter consists of fibers called axons that allow brain cells to communicate with one another. The white matter is necessary for normal brain function. Read more...
Researchers from the United States and People's Republic of China ...Therapeutics Daily (subscription) (press release) - Newtown,PA,USA... According to a study from the United States, "Passive immunization of murine models of Alzheimer disease amyloidosis reduces amyloid-beta peptide (A-beta ...
Monoclonals expand into neural disordersNature.com (subscription) - London,England,UK... at least two dozen companies are also pursuing immunotherapies for Alzheimer. Most use active immunization, in which a small part of the beta-amyloid plaque is ...
Studies from Eli Lilly & Company highlight recent researchTherapeutics Daily (subscription) (press release) - Newtown,PA,USA... and improves memory in a murine model of Alzheimer disease (AD). ... the amyloid cascade hypothesis of AD pathogenesis postulates that amyloid beta (Abeta) peptide ...

Chocolate may boost brain power
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By Megan Rauscher
NEW YORK (Reuters Health) - Chocolate lovers rejoice. A new study hints that eating milk chocolate may boost brain function.
"Chocolate contains many substances that act as stimulants, such as theobromine, phenethylamine, and caffeine," Dr. Bryan Raudenbush from Wheeling Jesuit University in West Virginia noted in comments to Reuters Health.
"These substances by themselves have previously been found to increase alertness and attention and what we have found is that by consuming chocolate you can get the stimulating effects, which then lead to increased mental performance."
To study the effects of various chocolate types on brain power, Raudenbush and colleagues had a group of volunteers consume, on four separate occasions, 85 grams of milk chocolate; 85 grams of dark chocolate; 85 grams of carob; and nothing (the control condition).
After a 15-minute digestive period, participants completed a variety of computer-based neuropsychological tests designed to assess cognitive performance including memory, attention span, reaction time, and problem solving.
"Composite scores for verbal and visual memory were significantly higher for milk chocolate than the other conditions," Raudenbush told Reuters Health. And consumption of milk and dark chocolate was associated with improved impulse control and reaction time.
Previous research has shown that some nutrients in food aid in glucose release and increased blood flow, which may augment cognitive performance. The current findings, said Raudenbush, "provide support for nutrient release via chocolate consumption to enhance cognitive performance."

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Different Forms Of Amyloid Beta In Alzheimer's Disease
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Researchers at UC Irvine have shown that different forms of amyloid beta lead to neural damage in different ways, leading to an increasingly complex view of amyloid toxicity in the Alzheimer brain. The finding could modify the way therapeutic approaches for the treatment of Alzheimer's disease are designed. The researchers studied the effects of different forms of the amyloid beta peptide on human brain cells. Amyloid beta accumulation is one of two hallmarks of Alzheimer's disease and is considered a major target for researchers looking into therapies for the treatment of the disease. After death, most amyloid beta found in the brains of Alzheimer's patients is in fibrillar form -- long, insoluble fibers bound together in deposits called senile plaques; however, there are also soluble forms of amyloid beta, or oligomers, that may decisively contribute to neural degeneration. The experiments conducted at UCI showed that the soluble forms of amyloid beta are much more toxic and lead to neuronal death in as little as 12 hours. The fibrillar form, meanwhile, does not actually kill the neurons, but slowly, over a period of 10 or more days, renders them useless. Not known is whether the soluble amyloid beta in the Alzheimer brain eventually turns into the fibrillar kind, or whether the two are completely different.

Key Stress Protein Linked To Toxicities Responsible For Parkinson's, Alzheimer's...