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

Tanzi Presents Progress at Mass General Hospital

Dr. Lee Schwamm, Vice-chairman of Neurology at MGH, led off the event acknowledging the exciting and breakthrough work Dr. Tanzi conducts at MGH. He was followed by Jim Thompson, Chief Development Office at MGH who thanked Cure Alzheimer’s Fund for the partnership with the hospital and the great efforts we are making together to end Alzheimer’s. Phyllis Rappaport, co-founder of Cure Alzheimer's Fund introduced Dr. Tanzi. Dr. Tanzi’s research has resulted in new genes that are revealing new information about the disease and significantly aiding researchers world-side in their efforts toward a cure.

Special Science Update from Cure Alzheimer's Fund

Science Update CoverThis Science Update gives you an overview about what is know about the science behind Alzheimer’s disease and how at Cure Alzheimer's Fund we are funding research to get to a cure as quickly as possible.

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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.

"Rock Stars of Science" Event a Huge Success!


Yesterday's Rock Stars of Science event in DC was a huge success. In front of a great audience, our own Rudy Tanzi brought home the point that strong support for Alzheimer's research is critical for finding a cure. He and the rest of the all-star line up of speakers urged Congress to increase funding for research and praised Congressional champions of research like MA Congressman Ed Markey.

But the event wasn't all serious. Rudy also took the stage with Aerosmith guitarist Joe Perry and NIH Director Francis Collins for a once in a lifetime performance.

We'll be bringing you more video from the event next week, so stay tuned.

For some great photos of the performance, CLICK HERE.

"Rock Stars of Science" Event Featuring Rudy Tanzi Today!

The "Rock Stars of Science" event, hosted by GQ Magazine, Geoffrey Beene Gives Back and Research!America is starting shortly, and we're very excited!

Our own Rudy Tanzi and Sam Gandy will be speaking about the progress we've made toward a cure for Alzheimer's and the urgent need for more research funding.

If we make a national commitment to finding a cure, we can end Alzheimer's by 2020. Join us today and help make it happen! - Just sign up on the form to the right.

If you couldn't make it to DC for today's event, you can participate online by following #rsos on Twitter.

We'll be tweeting about the event too: @CureAlzheimers

CAF's Rudy Tanzi interviewed about new Alzheimer's study

Yesterday, we posted about a new study showing that more than 35 million people worldwide are living with Alzheimer's Disease and other forms of dementia.

Cure Alzheimer's Fund's Rudy Tanzi, who is recognized as a leading expert on Alzheimer's Disease, was interviewed by Boston's NECN TV about the report and its implications. He stressed the critical importance of increased research funding to stop this disease.

Watch the interview here:

CAF's Rudy Tanzi interviewed about new Alzheimer's study

Yesterday, we posted about a new study showing that more than 35 million people worldwide are living with Alzheimer's Disease and other forms of dementia.

Cure Alzheimer's Fund's Rudy Tanzi, who is recognized as a leading expert on Alzheimer's Disease, was interviewed by Boston's NECN TV about the report and its implications.  He stressed the critical importance of increased research funding to stop this disease.

Watch the interview here:

New Report: 35 million suffer from dementia worldwide - projected to reach 115 million by 2050

Today is World Alzheimer's Day, and the big news of the day is a report from Alzheimer's Disease International, which paints a grim picture of the future if this devastating disease goes unchecked. The report says that currently 35 million people worldwide suffer from Alzheimer's Disease - and that number is expected to double every twenty years, reaching 115 MILLION Alzheimer's and dementia sufferers by 2050.

Here's an excerpt from the report:

Not only are the numbers reason for concern, but Alzheimer's disease and dementia have an enormous impact on societies; it can be called an epidemic that is increasing its pace with the "graying" of the population around the world. Poor recognition, underdiagnosis and stigma cause significant problems for people with dementia and their families in countries of all sizes and communities of all income levels.

The ADI report also highlights the financial costs of dementia, which were estimated to be over $300 billion in 2005 alone. These costs, currently borne mostly in the developed world, are also expected to skyrocket together with global rates of the disease. Already, the costs of caring for Alzheimerís and dementia patients consume over one quarter of the US Medicare and Medicaid budgets. If left unchecked, Cure Alzheimer's Fund's estimates suggest they could single-handedly bankrupt Medicare and Medicaid within the next decade.

We are dedicated to ensuring that this grim picture does not come to pass. We've made tremendous progress already, and we are working to find a cure by 2020. But to get there, we need your continued support. Please donate to help us find a cure and stop this devastating disease.

Rockstars of Science Hit Capitol Hill

Over the summer, we told you about an exciting honor for one of our lead researchers, Dr. Rudy Tanzi. Along with other leading scientists including NIH Director Francis Collins, Dr. Tanzi was named as one of GQ Magazine's "Rockstars of Science".


What is a "Rockstar of Science", you might ask? They're the doctors and researchers who are accelerating treatments and cures "from research bench to bedside". GQ brought together a star-studded list of musicians (like Aerosmith's Joe Perry,, and Sheryl Crow) and scientists (like Dr. Tanzi, Sam Gandy, and Francis Collins) for a fun and impactful photo shoot and feature story.

And, next week, Dr. Tanzi, Director Collins, and Joe Perry of Aerosmith are taking the "Rockstars of Science" campaign to Capitol Hill to talk about the importance of research funding for curing diseases like Alzheimer's. And they are going to play!

If you're in the DC area, don't miss this great event! If not, check back here next week for video and highlights.

Rock Stars of Science: September 24
11:30 a.m. to 3 p.m. ∙ Capitol Visitors Center Auditorium
Special Appearance: Aerosmith’s Joe Perry Tribute to Congressional Champions of Research
Moderated by: Terry Moran of ABC News’ Nightline

For more information, click here.

To RSVP for this free event, click here.


European Consortium proposes three new genes!

by Rudolph E. Tanzi, Ph.D.

Two new genome studies from Europe have proposed three additional genes that may influence risk for Alzheimer's disease (AD). The gene findings are the result of a large consortium study conducted in Europe and add further support to the role of beta-amyloid in AD. While the three new genes exert only minor effects on AD risk (decreasing or increasing risk by only 15-20%), they should be helpful when combined with the roughly 100 genes previously identified in the Cure Alzheimer's Fund Alzheimer's Genome Project (AGP) for furthering our understanding of this disease. The new genes as well as the dozens of others identified over the past two decades are summarized on Cure Alzheimer's Fund-supported online Alzheimer's gene encyclopedia and database,

The initial publication of the results of Cure Alzheimer's Fund’s AGP (Bertram et al., 2008), was named by Time magazine as a "Top Ten Medical Breakthrough of 2008". The updated list of now over 100 genes that influence risk for AD from the AGP and other's studies, including the three described in the two new reports from the European Consortium, join the four previously established AD genes discovered between 1987 and 1995, three of which were co-discovered by Cure Alzheimer's Fund Research Consortium Chairperson, Dr. Rudy Tanzi of Harvard Medical School and Massachusetts General Hospital. The combination of all of these genes will be invaluable in driving our progress toward a cure for AD.

At Cure Alzheimer's Fund, we believe that AD will ultimately be conquered by a combination of "early prediction" and "early prevention" of this devastating disease . In both cases, we need to know the complete set of genes that influence one's risk for AD. The complete battery of AD genes will someday be used to both predict one's lifetime probability of getting AD, and to guide research aimed at obtaining a clearer understanding of the causes of AD and developing effective new therapies for AD.

In summary, while the three new AD genes described in the two new European studies exert only modest effects on AD risk, when added to the roughly 100 other AD genes previously identified in the Cure Alzheimer's Fund AGP and other AD genetic screens, we will hopefully move a step closer to our ultimate goal of beating AD with "early prediction-early prevention.”

Rudolph E. Tanzi, Ph.D.
Joseph P. and Rose F. Kennedy
Professor of Neurology,
Harvard Medical School
Director, Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease Massachusetts General Hospital
114 16th Street Charlestown, MA 02129
(T) 617-726-6845 (F) 617-724-1949