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

New Report: Muscle Weakness Linked to Alzheimer’s Risk in Elderly

Numerous media outlets have posted stories in recent days on the research conducted by Rush University Medical Center which found that elderly people with weak muscles may be at an increased risk for Alzheimer's disease.


Rush University researchers followed 970 older adults (average age of 80) who did not have dementia and during the 3-4 year follow-up period, 14% developed Alzheimer’s. Those individuals with the highest levels of muscle strength at the start of the study were 61% less likely to develop Alzheimer’s.


Cure Alzheimer’s Fund has also suppoted research in this area and has found that weak muscles, possibly resulting from stroke, could be another indication of the onset of Alzheimer’s. Research has already established links between stroke and Alzheimer’s. For more information, see a study by Giuseppina Tesco et al in Neuron, 2007: 54(5): 721-37 supported by Cure Alzheimer’s Fund.


Read the full article

Other studies have also shown the positive effects of exercise in slowing the onset of Alzheimer’s which suggests that muscle strength in certain populations may be an indicator of the presence or onset of Alzheimer’s disease.


For more information on the role exercise plays in reducing your risk of Alzheimer’s, check out CAF’s Dr. Sam Sisodia’s article titled, “Can Exercise Help Prevent Alzheimer’s?”

Read the full article


Cure Alzheimer’s Fund is proud to present a total of 25 published papers that result from our funding and support. Our researchers are making significant progress, but we need your support. Please donate today to help us find a cure.

New Study Claims Inflammation and High Blood Pressure Are Risk Factors for Late-Onset Alzheimer’s

A new study published in November’s Archives of General Psychiatry titled, “Vascular Factors and Markers of Inflammation in Offspring With a Parental History of Late-Onset Alzheimer Disease,” suggests that Alzheimer’s is partly driven by two preventable risk factors: inflammation and high blood pressure.


Danish researchers studied 206 volunteers whose parents had developed dementia late in life and found that the volunteers were more likely to have high blood pressure and a high level of inflammatory proteins (or cytokines) than those whose parents did not have Alzheimer’s.


While these researchers note that 60 percent of an individual's Alzheimer's risk appears to be driven by genes, the individual’s lifestyle factors may play a more significant role than once thought. Therefore, the study claims that early interventions could prevent late-onset Alzheimer’s such as screenings for hypertension, inflammation and clogged arteries.


To learn more, check out a paper by Basavaraj V Hoolie and Rudy Tanzi of Massachusetts General Hospital, supported by Cure Alzheimer’s Fund. Titled “A Current View on Alzheimer’s Disease.” Tim Armour, President of Cure Alzheimer's Fund explains:


Inflammation has long been associated with Alzheimer’s disease, and to the extent that individuals with a family history of the disease are prone to hypertension and other aspects of inflammation, appropriate prophylactic measures may be appropriate.

For more information on research sponsored by Cure Alzheimer’s Fund, visit us at

Fred Hassan on Alzheimer’s Disease - “Biggest Long-Term Health Challenge”

In a blog post featured on the Huffington Post last month, Fred Hassan, CEO of Schering-Plough Corporation, called Alzheimer’s disease our nation’s greatest long-term health challenge – and we could not agree more.

Hassan is taking a stand, demanding that Congress makes Alzheimer’s a part of the national dialogue on
health care. In case you missed it, an excerpt is below:

We must begin somewhere to turn health care reform from ideas into good policies and actions. Through a national crusade on Alzheimer's, we can rally as Americans around our biggest long-term health care challenge. What we learn from that can help us get other things right. And when we look in the mirror as a nation that wants to care for its weakest citizens, we will like what we see.

Read the entire article 

As the health care debate grows, we must make sure every member of Congress knows that by investing $5 billion per year on research over the next 10 years, we can find a cure.

Sign our letter
and stand with Cure Alzheimer’s Fund. Urge Congress to support increased funding for Alzheimer’s research in health care reform and help find a cure by 2020.

Dr. Tanzi Presents "Alzheimer's Disease: From Genes to Novel Therapeutics" at the University of Pittsburgh School of Health

At the University of Pittsburgh’s School of Public Health last month, Dr. Rudolph Tanzi, Lead Scientist at the Cure Alzheimer’s Fund Research Consortium, spoke as part of the prestigious Jay L. Foster Memorial Lecture Series on Alzheimer’s Disease.


To view Dr. Tanzi’s presentation titled, “Alzheimer’s Disease: From Genes to Novel Therapeutics,” click on the link below.


Alzheimer’s Disease: From Genes to Novel Therapeutics 


The slide show will walk you through a timeline of Alzheimer's disease genetics, discussing the discoveries and breakthroughs of the genetic mutations related to Alzheimer's disease. The presentation focuses on addressing the problem at the root, more fully comprehending the Alzheimer's genes and the superiority of a personalized medicine approach to combating the disease. 

Dr. Tanzi’s presentation demonstrates to all our supporters the progress and vital importance of the Cure Alzheimer’s Fund Research Consortium. Take a minute and view the presentation for yourself.


We've made tremendous progress already but we need your continued support. Please donate to help us find a cure and stop this devastating disease.