Find updates on the work of our researchers here, as well as news about recent advances in Alzheimer's science, funding and awareness.

Federal Funding to Support Cure Alzheimer’s Fund in 2010!

Earlier this week, President Obama signed a bill into law that includes $150,000 in federal funding to support our search for a cure!

Submitted as part of the Consolidated Appropriations Act of 2010 by Sens. John Kerry and Paul Kirk, and Rep. Ed Markey, the funding will support the Alzheimer’s Genome Project and provide state-of-the-art equipment for research.


Tim Armour, President and CEO of Cure Alzheimer’s Fund, expressed his gratitude saying:


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. 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.


5.2 million Americans currently battle Alzheimer’s, but with a national commitment to cure this disease, we can get there in 10 years. We can stop this disease in its tracks.


To learn more about what we are doing to find the cure, check out our roadmap to a cure:


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





Happy Holidays!

During this holiday season, we would like to say thank you for everything you have done this year to help us in our search for a cure. As you know, our ability to fight this disease comes from each and every one of you!

We are the only organization with a clear roadmap to a cure – and we are working harder than ever to cure this terrible disease right now, not years from now.

That’s why this holiday season, we launched our year-end fundraising drive -- $30,000 in 30 days in first-time donors -- and your response has been remarkable. It’s because of people like you that we are able to fund the research that will ultimately cure this disease – but there is so much more we can do!

This holiday season, please consider making a contribution to the Cure Alzheimer’s Fund – there is no better gift than saving lives.

What we are trying to accomplish together is nothing short of amazing – a cure for Alzheimer’s now.

And, it is within our sight.

We have the roadmap to get there, now we need your help to fund it.

We hope you will consider making a contribution to our fight against this disease, and together, we will prevent the next generation from ever having to fear a future with Alzheimer’s.

Wishing you and your family a joyous holiday,

Tim Armour

President and CEO, Cure Alzheimer’s Fund


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











Dr. Rudy Tanzi: Partnering for Cures Video

On December 3rd, Cure Alzheimer’s Fund’s Rudy Tanzi took part in a panel discussion on breakthrough science at the Partnering for Cures meeting.

Partnering for Cures brought together philanthropy, medical research foundations, and the biotechnology and pharmaceutical industries in an effort to create collaborations for the development of new medical solutions.

The panel discussed the vital role philanthropic investment plays in supporting breakthrough science and Dr. Tanzi's presentation echoed this sentiment, thanking Cure Alzheimer's Fund for its support of the Alzheimer's Genome Project!

Dr. Tanzi's presentation focused on the importance of genetics and genomics in the search for a cure. He emphasized that technological advances are improving the understanding of the genetic mechanism that controls Alzheimer's disease and are making it possible to identify the complete set of genes influencing risk for this devastating disease. Tanzi emphasized that the more authentic disease-related genes we identify, the more rapidly and accurately we will be able to predict the probability of the disease in each person, detect the beginnings of pathology and prevent or delay it from taking hold, and treat it successfully in those who have already been stricken.

The panel also included presentations from: James Greenwood, President and CEO of BIO; Mara Aspinall, President and CEO of On-Q-ity; Stephen Friend, President, CEO and Co-Founder of Sage Bionetworks; Levi Garraway, M.D., Ph.D., Department of Medical Oncology at the Dana-Farber Cancer Institute; and Garry Neil, Corporate Vice President of Johnson & Johnson.

Want to learn more? Click on the link below to watch the complete panel discussion:

Letter from the Founders - Why You Should Care About Alzheimer's Research

Why should you care about Alzheimer’s research?

Currently, for every dollar spent on Alzheimer's care, only a penny is spent working toward a cure. This is a bad equation for a disease that is estimated to cost more than $100 billion in care (Medicare and Medicaid alone) in 2009.

Robert Malinow Joins Research Consortium

Professor, Section of Neurobiology, UCSD,

Professor of Neurosciences, UCSD

Shiley Chair in Alzheimer’s Disease Research in Honor of Dr. Leon Thal

Dr. Malinow’s research is directed toward understanding how the brain forms and stores memories. His laboratory examines how neuronal activity controls the strength of communication between neurons, at sites called synapses. Synapses are key sites affected by diseases of cognition. Synaptic plasticity, or the ability of the connection between neurons to vary, is thought to underlie the formation and storage of memories. It is thought that a detailed understanding of synaptic plasticity will identify critical steps that may be the targets of diseases such as Alzheimer’s disease. Such an understanding eventually may lead to treatments that prevent the disease.

Cure Alzheimer’s Fund Research Consortium is made up of leading Alzheimer’s researchers who serve on a voluntary basis. The Consortium helps guide the Cure Alzheimer’s Fund Research Roadmap and pursue research that will lead to a cure.


Leveraging Donations is Working

Rob Moir and Guiseppina Tesco Awarded Prestigious Research Project Grants as a Result of Cure Alzheimer’s Fund Start-up Funding

A big win by Cure Alzheimer’s Fund has come by investing small amounts of money in what some deem as more risky research. These research ideas often are very innovative and therefore not appealing to traditional funding sources.


However, Cure Alzheimer’s Fund’s entrepreneurial approach and ability to nimbly provide funding in an efficient manner allow us to purse this potentially groundbreaking work. And it’s paying off. We invest in the early-stage research, giving researchers the opportunity to better understand their research hypotheses and to gather preliminary results, setting the stage for them to apply for much larger government grants.


Two Cure Alzheimer’s Fund researchers, Rob Moir of Massachusetts General Hospital and Guiseppina Tesco of the Department of Neuroscience at Tufts University School of Medicine, have accomplished exactly this.


Dr. Moir’s work is focused on the concept that Abeta, a peptide shown to be a primary initiator of Alzheimer’s pathology, is an antimicrobial peptide and part of the innate immune system. His early work on this subject, funded by Cure Alzheimer’s Fund, just resulted in a research project grant (R01). An RO1 is the original and historically oldest grant mechanism used by the National Institutes of Health. The R01 provides support for health-related research and development.


Dr. Tesco has done pioneering work in the relationship between traumatic brain injury and Alzheimer’s. After her initial paper on the topic in the journal Neuron in 2007, Cure Alzheimer’s Fund supported her continued pilot studies, leading to her recent award of two RO1 grants for major studies in this field.


Study Shows Sleep Loss Linked to Increase in Alzheimer’s Plaques

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

They 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 compounds it interacts with may become new drug targets for treatment of Alzheimer's disease," says senior author 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. "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's laboratory 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.

Jae-Eun Kang, Ph.D., a post-doctoral fellow in Holtzman's lab, 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 led by Randall Bateman. M.D., assistant professor of neurology and a neurologist at Barnes-Jewish Hospital, also showed that amyloid beta levels were generally higher when subjects were awake and lower when they slept.

To confirm the link, Kang learned to use electroencephalography (EEG) on the mice at the Sleep and Circadian Neurobiology Laboratory at Stanford University with researchers Seiji Nishino, M.D., Ph.D., and Nobuhiro Fujiki, M.D. Ph.D. 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 where John Cirrito, Ph.D., 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 they weren't caused by the stress of sleep deprivation, according to Holtzman.

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

Miranda M. Lim, M.D., Ph.D., a neurology resident and post-doctoral researcher in Holtzman's lab, performed long-term behavioral experiments with the mice. She 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. Holtzman also plans to learn more of the molecular details of how orexin affects amyloid beta.

"We would like to know if there are ways to alter orexin signaling and its effects on amyloid beta without necessarily modifying sleep," he says.

Additional studies will address the questions of whether increased amyloid beta during wakefulness is connected to increased synaptic activity and whether some aspect of sleep lowers amyloid beta levels independent of synaptic activity.

Happy Thanksgiving!

Happy Thanksgiving, everyone!


It is during this special time of year that we think about our blessings and are reminded that the lives that touch ours are our greatest asset. After all, Thanksgiving is about spending time with the ones we care about most and giving thanks for the health and happiness of our loved ones.


Unfortunately, not everyone is privileged to count health as one of their blessings this holiday season. In fact, every 70 seconds another American is diagnosed with Alzheimer’s -- that is 5.4 million Americans and 35 million people worldwide inflicted with this devastating disease.


With 78 million Baby Boomers quickly approaching the age of greatest risk for Alzheimer’s, we must find a cure fast – and that’s exactly what we are working on.


Cure Alzheimer’s Fund is the only organization with a roadmap to the cure. We are addressing the Alzheimer’s crisis head-on, conducting research aimed at finding the major causes of the disease and helping accelerate the developments of effective therapies and ultimately find a cure.


Everyday we make significant strides, bringing us that much closer to a cure, but we need your help.


Right now we are launching a last minute holiday fundraising drive -- $30,000 in 30 days to cure Alzheimer’s. Please consider donating to the Cure Alzheimer’s Fund this holiday season and making a contribution to our fight against Alzheimer’s.


On behalf of Cure Alzheimer’s Fund, I want to wish you a happy Thanksgiving! May you spend this special day with your family and friends and enjoy the company of those that matter most.


Best wishes,


Tim Armour

President and CEO, Cure Alzheimer’s Fund