Press Releases

New Published Study Shows Russian Antihistamine Has Surprising Effects on the Amyloid Peptide: Cure Alzheimer's Fund Researcher Spearheading Research

Boston—A new study published in Molecular Neurodegeneration unexpectedly showed that a retired Russian hay fever drug, Dimebon, which has shown promise in improving and stabilizing cognition in Alzheimer’s disease, has the surprising effect of increasing the levels of beta amyloid peptide, a molecule that is tied to the development of Alzheimer’s. Previous work aimed at treating or preventing the devastating disease has focused on lowering levels of beta amyloid peptide.

Funded by Cure Alzheimer's Fund, the new studies on Dimebon, which is produced by Medivation, Inc., and now owned by Pfizer, Inc., were first announced on July 15 at the Alzheimer's Association 2009 International Convention on Alzheimer's Disease (ICAD 2009) in Vienna, Austria by Dr. Sam Gandy, Mount Sinai Professor in Alzheimer’s Disease Research at the Mount Sinai School of Medicine in New York NY and a member of the Cure Alzheimer’s Fund research consortium.

John Cirrito PhD, and David M. Holtzman, MD, Professor and Chairman of the Department of Neurology at Washington University in St Louis, St Louis, MO, joined Dr. Gandy in his research. Dr Holtzman is also a member of the Cure Alzheimer’s Fund research consortium.

The idea to study Dimebon and beta amyloid peptide arose from a clinical trial conducted in Russia that showed promising clinical benefits. The newly published experiments involved mice that carry human Alzheimer’s genes and develop brain protein structures that demonstrate the same characteristics as human Alzheimer's.

“This was quite an unexpected result, and there is still a lot of research to be done on Dimebon. I wouldn’t be surprised to see a different result in chronic dosing with the drug. But I am amazed to see such promise from a drug that origin

ally had nothing to do with Alzheimer’s,” Gandy said. “Bachurin and Hung (of Medivation) and their academic colleagues have shone a light on something that might help us to better understand this devastating disease and how to combat it.”

Since 1986, genetic evidence, largely the work of Rudolph Tanzi, PhD, Professor of Neurology and Genetics at Massachusetts General Hospital and Director of the Cure Alzheimer’s Fund Genetic Initiative, has linked every AD mutation to enhancement of beta amyloid buildup. Dr. Gandy’s research took a new approach to fighting that buildup, and, Gandy says, “The Dimebon story, however unexpected, does nothing to diminish the profound importance of amyloid in Alzheimer’s genetics.”

“Dr. Gandy’s work is remarkable, and we are lucky to have him as an ally in our battle against Alzheimer’s disease,” said Tim Armour, President and CEO of Cure Alzheimer’s Fund.

About Cure Alzheimer's Fund

Cure Alzheimer's Fund™ is a 501c3 public charity whose mission is to fund research with the highest probability of slowing, stopping or reversing Alzheimer's disease. Cure Alzheimer’s Fund is characterized by a venture approach to philanthropy, which targets funding to specific research objectives. All expenses and overhead is paid for by its founders and all contributions go directly to research. The Foundation has no financial or intellectual property interest in the research funded, and will make known the results of all funded research as soon as possible. Cure Alzheimer’s Fund is a national organization with offices in Boston and Pittsburgh. For more information, visit www.curealzfund.org.

 

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Cure Alzheimer’s Fund Receives Federal Funding to Support Promising Research on Genetic Causes, Cure for Disease

Washington, December 17, 2009 — President Obama this week signed a bill into law that includes funding to support the Boston-based Cure Alzheimer’s Fund’s efforts to find cure for Alzheimer’s disease.

Submitted as part of the Consolidated Appropriations Act of 2010 by Sens. John Kerry and Paul Kirk, and Rep. Ed Markey, Cure Alzheimer’s Fund was recognized for its work in the field of Alzheimer’s disease research and granted $150,000 in federal funding for state-of-the-art equipment for research.

 

“We thank Senators Kerry and Kirk, and the late Senator Kennedy and Congressman Markey for their efforts to acknowledge our work to make Alzheimer’s a distant memory,” said Tim Armour, president and CEO of Cure Alzheimer’s Fund. “Our goal is to find a cure within 10 years, and our research programs are the key to discovery. This federal funding shows our government is paying attention and dedicated to fighting this debilitating disease.”

 

The funding will support the “Alzheimer’s Genome Project” (AGP), part of the ambitious national research strategy set forth by Cure Alzheimer’s Fund to identify the causes and better understand the disease. Time Magazine/CNN saluted AGP as a “Top Ten Medical Breakthrough of 2008.”  Approximately 5.2 million Americans currently battle Alzheimer’s and the clock is ticking as the Baby Boomer generation approaches the at-risk age group.

 

Cure Alzheimer’s Fund™ is a 501c3 public charity established to fund targeted research with the highest probability of slowing, stopping or reversing Alzheimer’s disease.  For more information, please visit http://www.curealzfund.org.

 

 

 

 

 

 

 

 

 


 

CAF's David Holtzman's Study Shows Sleep Loss Linked to Increase in Alzheimer's Plaques

May Lead To New Treatments for Devastating Disease

Chronic sleep deprivation in mice with Alzheimer's disease type changes makes Alzheimer's brain plaques appear earlier and more often, researchers lead by Cure Alzheimer's Fund's Dr. David Holtzman at Washington University School of Medicine in St. Louis reported online this week in Science Express. The study was funded in part by Cure Alzheimer’s Fund.

 

The researchers also found that orexin, a protein that helps regulate the sleep cycle, appears to be directly involved in the increase.

Neurodegenerative disorders like Alzheimer's disease and Parkinson's disease often disrupt sleep. The new findings are some of the first indications that sleep loss could play a role in the genesis of such disorders.

"Orexin or pathways that it effects  may become new drug targets for treatment of Alzheimer's disease," says senior author David M. Holtzman, M.D., a member of Cure Alzheimer’s Fund Research Consortium. "The results also suggest that we may need to prioritize treating sleep disorders not only for their many acute effects but also for potential long-term impacts on brain health."

Holtzman, the Andrew and Gretchen Jones Professor and chair of the Department of Neurology at the School of Medicine and neurologist-in-chief at Barnes-Jewish Hospital, uses a technique called in vivo microdialysis to monitor levels of amyloid beta in the brains of mice genetically engineered as a model of Alzheimer's disease. Amyloid beta is a protein fragment that is the principal component of Alzheimer's plaques.

Holtzman's team noticed that brain amyloid beta levels in mice rose and fell in association with sleep and wakefulness, increasing in the night, when mice are mostly awake, and decreasing during the day, when they are mostly asleep.

A separate study of amyloid beta levels in human cerebrospinal fluid also showed that amyloid beta levels were generally higher when subjects were awake and lower when they slept.

To confirm the link, Holtzman’s team learned to use electroencephalography (EEG) on the mice at the Sleep and Circadian Neurobiology Laboratory at Stanford University. The EEG readings let researchers more definitively determine when mice were asleep or awake and validated the connection: Mice that stayed awake longer had higher amyloid beta levels.

"This makes sense in light of an earlier study in our lab showed that increases in synaptic activity resulted in increased levels of amyloid beta," Holtzman notes. "The brain's synapses may generally be more active when we're awake."

Depriving the mice of sleep caused a 25 percent increase in amyloid beta levels. Levels were lower when mice were allowed to sleep. Blocking a hormone previously linked to stress and amyloid beta production had no effect on these changes, suggesting that they weren't caused by the stress of sleep deprivation, according to Holtzman.

Researchers elsewhere had linked mutations in orexin to narcolepsy, a disorder that is characterized by excessive daytime sleepiness. The brain has two kinds of receptors for orexin, which is also associated with regulation of feeding behavior.

When Holtzman's group injected orexin into the brains of the mice, mice stayed awake longer, and amyloid beta levels increased. When researchers used a drug called almorexant to block both orexin receptors, amyloid beta levels were significantly lower and animals were awake less.

Holtzman's team performed long-term behavioral experiments with the mice. They found that three weeks of chronic sleep deprivation accelerated amyloid plaque deposition in the brain. In contrast, when mice were given almorexant for two months, plaque deposition significantly decreased, dropping by more than 80 percent in some brain regions.

"This suggests the possibility that a treatment like this could be tested to see if it could delay the onset of Alzheimer's disease," says Holtzman.

Holtzman notes that not only does the risk of Alzheimer's increase with age, the sleep/wake cycle also starts to break down, with older adults progressively getting less and less sleep. Investigators are considering epidemiological studies of whether chronic sleep loss in young and middle-aged adults increases risk of Alzheimer's disease later in life.

"We would like to know if there are ways to alter orexin signaling and its effects on amyloid beta without necessarily modifying sleep," Holtzman said in hopes of learning more of the molecular details of how orexin affects amyloid beta.

“We are always impressed by the ingenuity of the Cure Alzheimer’s Fund Consortium scientists.  Dr. Holtzman and his team have done remarkable work that could prevent the onset of Alzheimer’s disease for millions of Americans,” said Tim Armour, President and Chief Executive Officer of the Cure Alzheimer's Fund. “We are optimistic that these findings will bring us closer to understanding and finding a cure for this devastating disease.”

Long dedicated to Alzheimer’s research, Cure Alzheimer’s Fund has set forth an ambitious and aggressive national research strategy setting a 10-year goal for the development of effective therapies and discovery of an eventual cure for this devastating disease.

In addition to the Cure Alzheimer’s Fund, the National Institutes of Health, the NIH Neuroscience Blueprint Center Core Grant, the Alzheimer's Association Zenith Award and Eli Lilly supported this research.

Cure Alzheimer's Fund's Dr.Tanzi Briefs Congress on Research Progress, Rep. Markey Praises Fund

Washington – With more than 5 million Americans now living with Alzheimer’s disease, a 10 percent increase since 2002, medical researchers are in a sprint to map and sequence the genes susceptible to Alzheimer’s in hopes of leading to more aggressive therapeutic interventions to slow, stop or even reverse the effects of the disease.

Senate Appropriations Committee’s Commitment To Alzheimer’s Research Wins Plaudits

Cure Alzheimer’s Fund Urges Congress to Pass Bill This Fall

Boston—Praising lawmakers for recognizing the importance of finding a cure for Alzheimer’s Disease, Cure Alzheimer’s Fund commended the U.S. Senate Appropriations Committee for passing promising legislation with strong funding and language backing Alzheimer’s research. 

 

“We applaud the Committee for their support and call for more research and discovery in the field of Alzheimer’s,” said Tim Armour, President and CEO of Cure Alzheimer’s Fund. “With 5.2 million Americans currently battling this devastating disease and many Baby Boomers reaching the at-risk age, research is critical to better understand Alzheimer’s in hopes of finding more effective treatments and preventing this disease.”

The appropriations are part of the Departments of Labor, Health and Human Services, and Education, and other related agencies, for the 2010 Fiscal Year.

Advancements in the research could lessen the growing burden— both financial and emotional— that Alzheimer’s puts on society. In 2004, 25 percent of the combined Medicare and Medicaid expenses (about $122 billion) went to Alzheimer’s care.  Alzheimer’s alone could single-handedly bankrupt Medicare and Medicaid within the next decade if left unchecked.

Dedicated to Alzheimer’s research, Cure Alzheimer’s Fund has set forth an ambitious and aggressive national research strategy setting a 10-year goal for the development of effective therapies and discovery of an eventual cure for this devastating disease.

“When President Kennedy challenged our nation to land on the moon by the end of the 1960s, we met that challenge with fervor. Finding a cure for Alzheimer’s is no less daunting, but with the advances in research and technology it is in our reach,” said Armour. “This renewed dedication and commitment to research from Senate appropriators is a encouraging step toward reaching that goal.

“We urge the full Senate and House to remain supportive of this bill as it moves through the legislative process this fall,” Armour continued.  “It could help change the lives of the millions of Americans and their families struggling with this devastating disease today.”

 

Cure Alzheimer's Fund Study Finds Surprising Side Effect from New Alzheimer's Treatment

Dimebon looks clinically promising in Russian study,
now revealed to increase substance in brain implicated in disease causation

New findings, announced on July 15 at the Alzheimer's Association 2009 International Convention on Alzheimer's Disease (ICAD 2009) in Vienna, Austria, unexpectedly showed that the former hay fever drug Dimebon increases generation by the brain of the beta amyloid peptide, a substance implicated in causation of Alzheimer’s. A study from Russia, announced last year, suggested that Dimebon might improve and stabilize thinking ability in Alzheimer’s disease.

Cure Alzheimer's Fund Study Finds Surprising Side Effect from New Alzheimer's Treatment

Dimebon looks clinically promising in Russian study,
now revealed to increase substance in brain implicated in disease causation

New findings, announced on July 15 at the Alzheimer's Association 2009 International Convention on Alzheimer's Disease (ICAD 2009) in Vienna, Austria, unexpectedly showed that the former hay fever drug Dimebon increases generation by the brain of the beta amyloid peptide, a substance implicated in causation of Alzheimer’s. A study from Russia, announced last year, suggested that Dimebon might improve and stabilize thinking ability in Alzheimer’s disease.

Helmsley Trust Awards $300,000 Grant to Cure Alzheimer's Fund

Leona M. and Harry B. Helmsley Charitable Trust announced today it has awarded a $300,000 grant to Cure Alzheimer’s Fund.

Three Winners of New Award for Younger Researchers Announced by Coalition of Alzheimer Organizations

Annual Awards Support “Tomorrow’s Leaders in Alzheimer’s Disease Research;”

Honor Legacies of Drs. George Glenner and Leon Thal

April 9, 2008 – A coalition of leading Alzheimer’s disease organizations today announced the first three recipients of “Tomorrow’s Leaders in Alzheimer’s Disease Research” prizes; a new award mechanism to recognize outstanding young scientists in Alzheimer’s and dementia research.

Gene scan of Alzheimer's families identifies four new suspect genes

The first family-based genome-wide association study in Alzheimer’s disease has identified the sites of four novel genes that may significantly influence risk for the most common late-onset form of the devastating neurological disorder.