Promising treatment for Alzheimer's

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WVU finds promising treatment for Alzheimer's

Researchers take potential first step to cure brain degeneration

By Veronica Nett

The Charleston Gazette

CHARLESTON, W.Va.-- West Virginia researchers have found a promising treatment that might reverse the debilitating effects of Alzheimer's disease, and offer the first step toward a potential cure for the more than 5 million Americans who suffer from it.



In a study published this month in the Journal of Neuroscience, researchers at the Blanchette Rockefeller Neuroscience Institute have found the potential root cause of Alzheimer's, and a way to treat the symptoms of the disease.





The degeneration of synapses -- the point of connection between two nerve cells -- in the brain plays a critical role in the development of dementia in Alzheimer's patients, said Dr. Daniel Alkon, co-author of the study and scientific director of the BRNI at the West Virginia University Robert C. Byrd Health Sciences Center.





For decades, though, the thrust of research and pharmaceutical development has not been toward synapses loss but trying to reduce the amyloid plaques and neurofibrillary tangles - twisted fibers found inside the brain's cells - that form in the brain after the loss of synapses, Alkon said.





"Alzheimer's disease is not primarily a disease of plaques and tangles, as many had previously concluded," Alkon said. "It is most importantly a disease of synapses."





Alkon and his team are the first to achieve a fundamental molecular understanding of how synapses are lost in Alzheimer's patients before the plaques and tangles develop.





"In a way, I think we have the first comprehensive picture of the cause of this disease," Alkon said. "We're virtually looking at the entire picture. We're not looking at one aspect, not the plaques or the tangles or the synapses, we're looking at all of it, and by treating the target, we treat everything at once."

By targeting synapses loss, researchers have found a potential way to stop the development of plaques and tangles in the brain that contribute to dementia and other hallmarks of Alzheimer's, "virtually eliminating all other elements of the disease," Alkon said.

Researchers found that the use of Bryostatin and similar compounds target the enzyme PKCe, which controls the creation of synapses at the molecular level, Alkon said.






The compounds promoted the growth of new synapses and preserved existing synapses in the brain, Alkon said. They also stopped the decrease of PKCe and the increase of soluble Beta amyloid, meaning that the treatments could be used to prevent formation of plaques and tangles in the brain, he said.





The neuroscience institute has received approval to begin clinical testing of Bryostatin to treat the symptoms of Alzheimer's, and will begin testing in the next several months.





Researchers at the institute also are developing a skin test to identify Alzheimer's in patients during the early stages of the disease.





"Detection early and a vaccine to stop degeneration -- it's a potential cure, Alkon said."





The synaptogenic drugs designed by researchers at the institute also have potential in the treatment of traumatic brain injury and stroke, Alkon said.





"The potential is great," Alkon said. "We need to get clinical trials going. We feel the sooner we can get this to the patients, the better."

Rethinking Alzheimer's disease and its treatment targets

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PhysOrg.com) -- Psychiatry professor George Bartzokis introduces a new theory about the fundamental cause of Alzheimer's and other neurodegenerative diseases.

The standard explanation for what causes Alzheimer's is known as the amyloid hypothesis, which posits that the disease results from of an accumulation of the peptide amyloid beta, the toxic protein fragments that deposit in the brain and become the sticky plaques that have defined Alzheimer's for more than 100 years.

Billions of dollars are spent yearly targeting this toxic peptide — but what if this is the wrong target? What if the disease begins much earlier, fueled by a natural process? Reporting in the current edition of the journal Neurobiology of Aging, UCLA professor of psychiatry George Bartzokis argues just that and says that a better working hypothesis is the "myelin model."

"The greatest promise of the myelin model of the human brain is its application to the development of new therapeutic approaches," Bartzokis said.

Like insulation around wires, myelin is a fatty sheath that coats our nerve axons, allowing for efficient conduction of nerve impulses. It is key to the fast processing speeds that underlie our higher cognitive functions and encoding of memories.

But the lifelong, extensive myelination of the human brain also makes it uniquely vulnerable to damage. The myelin model's central premise is that it is the normal, routine maintenance and repair of myelin throughout life that ultimately initiates the mechanisms that produce degenerative diseases like Alzheimer's. That is, the amyloid-beta peptide and the tau peptide, which is also implicated in Alzheimer's, as well as the signature clinical signs of the disease, such as memory loss and, ultimately, dementia, are all byproducts of the myelin breakdown and repair processes.

"The pervasive myelination of our brain is the single most unique aspect in which the human brain differs from other species," said Bartzokis, who is a member of the Laboratory of Neuro Imaging in the UCLA Department of Neurology and a member of UCLA's Brain Research Institute. Myelin is produced by oligodendrocytes, specialized glial cells that themselves become more vulnerable with age.

Bartzokis notes that myelination of the brain follows an inverted U-shaped trajectory, growing strongly until our 50s, when it very slowly begins to unravel as we age. The myelin that is deposited in adulthood ensheaths increasing numbers of axons with smaller axon diameters and so spreads itself thinner and thinner, Bartzokis said. As a result, it becomes more susceptible to the ravages of age in the form of environmental and genetic insults and slowly begins to break down faster than it can be repaired.

The exclusive targeting of the amyloid-beta peptide for many years is understandable because the same genes and enzymes involved in controlling myelination and myelin repair are, ironically, also involved in the production of amyloid-beta proteins. Bartzokis' point is that the amyloid beta may actually develop as a result of the natural process of the repair and maintenance of myelin.

"So the breakdown that leads to Alzheimer's and other age-related brain diseases, such as Parkinson's, may begin much earlier, before the formation of the protein deposits that are used to define these diseases," Bartzokis said.

Most drugs being developed for Alzheimer's are targeting amyloid beta, but little if any clinical improvement is being seen. This is, according to Bartzokis, "similar to cleaning up a house that's been flooded by water but never repairing the actual pipe that created the flood.

"For drug development then, the targets should be much further upstream, earlier in the process before the AB plaques even develop," he said.

Instead of focusing on reducing amyloid beta, Bartzokis argues, the myelin model suggests entirely different approaches to treatment and prevention of Alzheimer's disease that precede plaque formation. With modern brain imaging technology, clinicians could track the dynamic changes taking place in the brain and intercede well before any signs of Alzheimer's are seen.

"With earlier intervention," Bartzokis said, "we could reduce and potentially eliminate the increasingly catastrophic burden of dementia on the individual and their family, the health care system, and our society."

You can make a difference in Alzheimer's research

Alzheimer Research Funding - Subcommittee Action
Your voice can make a difference.

Advocacy is a major component of the Alzheimer's Association mission. Advocates are people with Alzheimer's and related disorders, caregivers, friends and families whose voices together are a powerful tool for change and hope of a future without Alzheimer's.

Alzheimer advocates are calling for advancements in research and enhanced care and support at the federal, state and local levels. The payoff has been phenomenal to date: substantial increases in federal research funding, growth in state-supported services and improvements in the quality of care for those in nursing homes.
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Exercise May Cut Risk of Dementia

A Study Shows Physical Activity in Middle Age Has Brain Benefits Years in the Future

WebMD Health News Exercising in middle age may help ward off dementia and Alzheimer's disease decades later.

In a study of more than 1,400 adults, those who were physically active in their free time during middle age were 52% less likely to develop dementia 21 years later than their sedentary counterparts. Their chance of developing Alzheimer's disease was slashed even more, by 62%.

These patterns were even stronger in people with the ApoE e4 gene, which is associated with higher risk of developing Alzheimer's disease.

"By being physically active in midlife, people who carry the ApoE e4 gene can lower their risk of Alzheimer's to the same level as someone not carrying the gene," says researcher Suvi Rovio, MSc, of the Karolinska Institute in Stockholm, Sweden

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Another reporting of Alzheimer's and dementia brain plaques cleared in mice

Protein accumulations, or plaques, characteristic of Alzheimer's disease can be eliminated from the brains of mice, researchers report, by encouraging scavenger immune cells called macrophages to do their work.
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Treating Chronic Infections May Block Alzheimer's and dementia

Treating Chronic Infections May Block Alzheimer's and dementia


Amsterdam – Researchers are breaking new ground in the emerging role of infection in the development of Alzheimer's.

A number of chronic diseases are in fact caused by one or more infectious agents. For example, stomach ulcers are caused by Helicobacter pylori, chronic lung disease in newborns and chronic asthma in adults are both caused by Mycoplasmas and Chlamydia pneumonia, while some other pathogens have been associated with atherosclerosis. The realization that pathogens can produce slowly progressive chronic diseases has opened new lines of research into Alzheimer’s disease.

In a special issue of the Journal of Alzheimer’s Disease published May 2008, guest editors Judith Miklossy, from The University of British Columbia, and Ralph N. Martins, from Edith Cowan University and Hollywood Private Hospital, Perth, Western Australia, and a group of experts explore this exciting topic. Alzheimer’s disease (AD), the most frequent cause of dementia, is a form of amyloidosis. It has been known for a century that dementia, brain atrophy and amyloidosis can be caused by chronic bacterial infections, namely by Treponema pallidum in the atrophic form of general paresis in syphilis. Bacteria and viruses are powerful stimulators of inflammation. It was suggested by Alois Alzheimer and his colleagues a century ago that microorganisms may be contributors in the generation of senile plaques in AD.

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Nature’s Bounty Vs. Dementia- More News

Is there promise of antioxidants from fruits and vegetables reversing Alzheimer's disease? Another study showing essentially the same thing. Titled "Molecules in Plants May Have Beneficial Effect on Alzheimer's Disease," this report was found on newswise.com. The article cites a study led by researchers the University of South Florida and Cedars-Sinai Medical Center which was published in Journal of Cellular and Molecular Medicine.
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Lipitor No Help for Dementia of Alzheimer’s Patients

April 18, 2008, 3:40 pm
Posted by Jacob Goldstein
More news from that big neurology meeting : Lipitor doesn’t help slow cognitive decline in Alzheimer’s patients, researchers said this week.

That’s something of a disappointment, given that it was a big, randomized study, and earlier data had showed promise. On the other hand, Alzheimer’s patients who took Lipitor at least didn’t seem to do any worse than those who took a placebo. All patients in the study also received Aricept, Pfizer’s Alzheimer’s drug.

Despite the fact that statins have been connected to anecdotal reports of memory problems, there were a few reasons to think the cholesterol drugs might help slow cognitive decline
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Drug Slows Alzheimer's Symptoms

A drug used to treat symptoms of moderate to severe Alzheimer's disease appears to be effective for one year, according to the results of a new multicenter study that provides additional support for the continuing effectiveness of the treatment, called Namenda®, for patients in the later stages of the disease (Archives of Neurology, January 2006).

"This study demonstrates that it is possible to alleviate some of the cognitive and functional losses associated with the later stages of Alzheimer's, providing a basis for greater optimism on the part of caregivers," said Barry Reisberg, MD, professor of psychiatry at NYU School of Medicine, the lead investigator of the study.

"Our study verifies that this medication continues to be beneficial and is safe with remarkably few side effects," said Dr. Reisberg, who is also Clinical Director of the Silberstein Aging and Dementia Research Center at NYU School of Medicine.

Namenda® was approved in October 2003 by the Food and Drug Administration for the treatment of moderate to severe Alzheimer's disease. The approval was based partly on a rigorous 28-week study of 252 people who were randomly chosen to receive the drug or a placebo. The results, published in the prestigious New England Journal of Medicine in the spring of 2003, showed that the drug could slow the downward spiral of the disease. Dr. Reisberg also was the principal investigator of this study.
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Memory Loss in Hyperactive State With Alzheimer's

FRIDAY, March 7 (HealthDay News) -- Memory loss, where the brain deletes inconsequential information, is in a hyperactive state in people with Alzheimer's disease, a new study suggests.

Researchers at California's Buck Institute for Age Research analyzed human brain tissue and found that people with Alzheimer's disease (AD) showed more signs of cleavage of a molecule called amyloid precursor protein (APP) than people without the disease.

But when they analyzed the brains of younger people without Alzheimer's, the researchers were surprised to find that they had about 10 times as much APP cleavage as Alzheimer's patients. However, younger brains make memories faster than they lose them.

The Buck Institute team believes that the malfunction of a biochemical switch associated with APP cleavage causes the brains of Alzheimer's patients to get stuck in the process of deleting memories. They added that this suggests the disease affects the plasticity or malleability of the brain.

The study was published in the March 7 issue of the Journal of Alzheimer's Disease.
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Brain games-Here is a challange

More and more research is confirming that keeping your mind active is extremely important in preventing dementia.

Prevention magazine is displaying games for you to play to sharpen your mind.
Try one or more of them. Then post which one you like the best or you feel is the most challanging

Click to go to mind games

New Helmet May Help Treat Alzheimer's Disease By Using Infrared Rays

Researchers now believe that they have found a promising new treatment for Alzheimer's disease, and it comes in the form of a helmet that shoots infrared rays into your head. It sound a little crude, but these researchers say that this treatment has worked on mice to help restore memory and stimulate brain cell growth, and they will now begin testing on humans.

If you ask me, this new Alzheimer's helmet looks a little bit like something out of science fiction movie, but if it works than who cares what it looks like. There's still a lot of testing to be done, says the inventor of this device Dr. Gordon Dougal from Durham University, before the Alzheimer's helmet is actually used to treat the disease - but early testing is very promising.
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New Year's Resolutions & Alzheimer's Prevention

New Year's Resolutions & Alzheimer's Prevention
Common New Year’s Resolutions Not Only Important for your Waistline, But for your Mind Too

Attention: Assignment Editor, Food/Beverage Editor, Health/Medical Editor, Lifestyle Editor, News Editor

TORONTO/ONTARIO/MEDIA RELEASE--(Marketwire - Jan. 1, 2008) - New Year's resolutions for healthy eating and increased activity are now more important than ever, say Alzheimer's experts. Your mind needs it too.

Research has shown that a good diet, in particular the Mediterranean diet high in monounsaturated "healthy" fats, and regular physical activity, are also important to keep Alzheimer's at bay.

Mental activities such as crossword puzzles are also helpful to prevent onset of dementias such as Alzheimer's disease.

"In addition to these lifestyle changes, there is really exciting research in the pipelines to be hopeful about in the future," says Dr. Nathan Herrmann, geriatric researcher and psychiatrist at Sunnybrook Health Sciences Centre. "We're involved in new and exciting trials that are investigating not only new medications to stop or slow down the accumulation of amyloid, but also new immunotherapy approaches through vaccines to help prevent or slow down the progression of the disease."

Amyloid is a sticky toxic protein that gradually deposits between nerve cells in the brain in Alzheimer's disease, damaging and killing cells. "It is important to stop this abnormal buildup," says Dr. Herrmann, also a Professor at University of Toronto. "It's possible these new approaches will become available within the next five to ten years."

January is Alzheimer's awareness month. An estimated 420,000 Canadians over 65 years have Alzheimer's disease or a related dementia. Alzheimer's is a progressive degenerative disease for which there is no preventive medicine or cure. It is characterized by a decline in mental abilities and changes in personality and behaviour. Usually there is a loss of functioning that eventually impedes the ability to carry out everyday activities. Alzheimer's disease is under-diagnosed and under-treated in Canada and worldwide.

Symptoms of Alzheimer's include: progressive loss of memory, difficulty with concentration, decrease in problem-solving skills and judgment, confusion and delusions, altered perception, impaired recognition, impaired skilled motor function, disorientation, impaired language skills and personality changes.

Sunnybrook Health Sciences Centre is transforming health care through the dedication of its more than 10,000 staff, physicians and volunteers who provide compassionate and innovative patient focused care. An internationally recognized leader in academic research and education and an affiliation with the University of Toronto distinguishes Sunnybrook as one of Canada's premier health sciences centres. Sunnybrook specializes in caring for newborns, adults and the elderly, treating and preventing cancer, disorders of the brain, mind and nervous system, cardiovascular disease, orthopaedic and arthritic conditions and traumatic injuries.

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*Please note: Dr. Herrmann can be made available for interviews on Wednesday, January 2nd.

/For further information: www.sunnybrook.ca/

Researchers Find Clue To Preventing Alzheimer's Disease

POSTED: 4:13 pm EST December 27, 2007
UPDATED: 4:32 pm EST December 27, 2007


Researchers may know why fish oil is helpful in preventing Alzheimer's disease.

Researchers at University of California, Los Angeles studied how a compound in fish oil, called Docosahexaenoic acid, or DHA, affects human brain cells and mice.

DHA appears to boost the production of a protein that destroys Alzheimer's-causing plaques.

DHA is found in fish oil supplements or fish like salmon.

Researchers are still trying to determine the most beneficial dose of DHA.

But, DHA may be most helpful for patients who haven't developed the disease yet.

Regular Walking Protects the Aging Brain

Elders and all interested in maintaining their brain should exercise by Susan Berg author of Adorable Photographs of Our Baby-Meaningful Mind Stimulating Activities and More for the Memory Challenged, Their Loved Ones and Involved Professionals, and long time dementia care practitioner

Study: Excessive Consumption of Sugary Drinks Linked Alzheimer's Disease

If you want to keep your mind sharp, you may want to lay off the soda. Excessive drinking of sugary beverages may increase the risk of Alzheimer's disease, according to a new study by the American Society for Biochemistry and Molecular Biology.

For the study, Dr. Ling Li, an assistant professor at the University of Alabama at Birmingham, and her colleagues tested whether high sugar consumption in an otherwise normal diet would affect Alzheimer’s progression.

Researchers used a genetic mouse model and over a 25-week period supplemented the regular
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Drug May Restore Memory With Alzheimer's Disease

Drug May Restore Memory With Alzheimer's Disease

Tuesday, November 13, 2007 9:06 AM

A 2006 study by MetLife found that adults over age 55 fear Alzheimer’s disease more than cancer, and with good reason. Alzheimer’s creeps up on patients and their families, robbing more than half of all Americans over age 85 of their memory and ability to care for themselves. But what is perhaps most frightening is that available treatments for the disease are by and large ineffective.


Research from Georgetown University several years ago suggested that a new class of anti-Alzheimer’s molecule, spirostenols, might undo some of the characteristic pathophysiology of Alzheimer-affected brains. Further testing showed that one such molecule, Caprospinol, actually reversed the course of an Alzheimer-like condition induced in rats. Today, Samaritan Pharmaceuticals (Las Vegas, NV), is gearing up for human clinical studies with this compound, also known as SP-233.


Buildup of beta-amyloid plaque in the brain has been recognized as a hallmark sign of Alzheimer’s for close to a century. Significant research points to this buildup as a causative factor in the development and progression of the disease. Until recently this hypothesis could not be tested definitively because of a lack of treatments that eliminate beta-amyloid plaques.


Samaritan Pharmaceutical scientists, working with leading researchers from Georgetown and McGill Universities, have demonstrated in a rat animal model, used to test new innovative drugs for Alzheimer’s disease, that Caprospinol clears amyloid plaque from the brain and restored memory. More impressively, treated rats perform as well or better in standardized behavioral tests than healthy control animals. In addition to eliminating plaque, Caprospinol appears to reverse the damage to memory and cognition that amyloid plaque causes.


Dr. Vassilios Papadopoulos, of McGill University Health Center, an adviser to Samaritan, and the discoverer of anti-Alzheimer’s spirostenols recently published a paper reviewing current development-stage approaches to treating Alzheimer’s disease (Recent Patents on CNS Drug Discovery, 2007, 2, 113-123). In this article, he identified amyloid plaque as a key target for therapy. The paper also summarized the research on acetylcholinesterase inhibitors as well as beta-amyloid aggregation inhibitors, of which Caprospinol is an example.


The rat studies were conducted by treating rats with a method of inducing an Alzheimer’s-like condition in test animals within four weeks. Rats treated in this fashion gradually lose cognitive skills, as well exhibiting a host of pathophysiologic brain changes indicative of Alzheimer’s. Then treatment of sick rats with Caprospinol brought about significant positive changes in brain pathology. Neuritic plaques, neurofibrillary tangles, astrogliosis, microgliosis, neuronal death, and tissue shrinking were all either reversed or markedly improved.


Why another Alzheimer’s drug?


One might ask why the world needs another Alzheimer’s disease drug. The answer lies in the relatively poor performance by existing Alzheimer’s medications.


Of the five Alzheimer’s disease drugs approved in the U.S., four (Razadyne®, Exelon®, Aricept®, and Cognex®) are inhibitors of cholinesterase, an enzyme that shuts down the activity of the neurotransmitter choline. Cholinesterase inhibitors are approved for mild to moderate Alzheimer’s. The fifth medication, Namenda®, is an antagonist of the N-methyl D-aspartate receptor which regulates glutamate, another neurotransmitter. None of these agents cure Alzheimer’s disease or significantly change the course of the disease. The best that some patients can expect is a delay in symptom progression and/or improvements in some memory and behavioral functions.


Enhancement of neurotransmitter activity is a logical approach to treating AD. However, there are problems with cholinesterase and glutamate-acting agents. The first is that they do not address the underlying pathology of Alzheimer’s, treating only the symptoms and not the disease. The second, related shortcoming is that the most responsive patients get worse. The positive benefits of drug treatment are, disappointingly, measured in weeks or at best, months. Alzheimer’s drugs also tend to be quite expensive, and organ toxicities are not uncommon.

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