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

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.

Founder Jacqui Morby Named Distinguished Daughter of Pennsylvania by Gov. Rendell

HARRISBURG, Pa., Oct. 21 -- Governor Edward G. Rendell and First Lady Judge Marjorie O. Rendell today recognized the accomplishments of eight Distinguished Daughters of Pennsylvania and praised their contributions to a variety of fields.

"This year's Distinguished Daughters of Pennsylvania have done extraordinary work in many different capacities," said Governor Rendell. "Their contributions to Pennsylvania and the nation have benefited everything from academics to athletics, the arts to the military, as well as businesses and communities. I am grateful for the work that these women have done on our behalf to strengthen our state and the quality of life for so many residents."

"It is a privilege to honor the dedication and commitment of these extraordinary women of Pennsylvania," said Judge Rendell. "Their legacy of leadership is making a difference across the state."

The following were honored as Distinguished Daughters: Juliet J. Goodfriend, Penn Valley; Judith R. Shapiro, Rosemont; Judith Joy Ross, Bethlehem; Eva Tansky Blum, Toi Derricotte and Jacqueline C. Morby, all of Pittsburgh; C. Vivian Stringer, Princeton, NJ; and Veronica Zasadni Froman, San Diego, CA.

To be selected as a Distinguished Daughter, women must be nominated by organizations within the state for accomplishments of statewide or national importance. Medals and citations are presented to honorees at the Governor's Residence in Harrisburg.

The Distinguished Daughters of Pennsylvania awards began in 1949 as a way to recognize influential women for their leadership, distinguished service, and contributions to the state through their professional and/or volunteer service. To date, 450 women have received the award and recognition.


Editor's Note: The following is a detailed list of this year's Distinguished Daughters of Pennsylvania.

.         Jacqueline Collins Morby, of Pittsburgh, is an innovator in the worlds of business and philanthropy. In 1988 Morby moved to Pittsburgh to open an office for TA Associates, a Boston-based private equity firm. In 2004 Morby co-founded the Cure Alzheimer's Fund which garnered Time Magazine and CNN 's designation in 2008 as one of the "Top 10 Medical Breakthroughs" in the world for its Alzheimer's Genome Project. A world traveler, Jacqui chairs the board of Population Action International.

.         Judith Joy Ross, of Hazelton, PA, is an internationally exhibited photographer known for her penetrating portraits of persons from all walks of life. Her most famous work to date is a collection of portraits, called "Portraits of the Hazleton Public Schools." The volume focuses on one of Ross's most personal series -- 67 portraits of students at public schools from her hometown of Hazleton. Between 1992 and 1994, Ross returned to the schools of her youth as a way of revisiting the experience of growing up. Shot with an 8 x 10-inch view camera, the photographs in Portraits are unpretentious and revealing in their psychological insight. They reveal the universally wonderful and terrifying rite of passage of going to school.

.         Judith Shapiro, of Rosemont, PA and New York City, is a distinguished scholar and academician. Shapiro is a cultural anthropologist who served as President of Barnard College from 1994 to 2008. Prior t that, she was o the faculty o the University o Chicago and Bryn Mawr, where she became the college's chief academic officer. She has been President o the American Ethnological Society and the Philadelphia Anthropological Society.

.         Juliet Goodfriend, of Penn Valley, PA, is the retired founder and President of Strategic Marketing Corporation, a global custom marketing research and consulting firm to the pharmaceutical industry. She created, and is president of Bryn Mawr Film Institute, the restored historic movie theater and film education center which serves 6000 members and provides a year-round program of movies and film courses for students of all ages. Her experience inspired her to help create NELI, the nonprofit executive leadership program at Bryn Mawr College. Goodfriend continues to address national audiences and undergraduates around the country as a Woodrow Wilson Visiting Fellow.

.         Veronica (Ronne) Froman, born in Uniontown, PA, currently resides in San Diego, CA. A graduate of Seton Hill University, she served in the United States Navy for 31 years and was in charge of naval bases and stations around the world. Froman retired from the Navy in 2001 with the rank of Rear Admiral. After retirement, Froman was instrumental in restoring confidence in the floundering local chapter of the American Red Cross after the 2003 southern California wildfires. She served as chief of business

operations for the San Diego Unified School District and in 2005 became the first chief operating officer for the city of San Diego. In 2007 she accepted another leadership position as senior vice president for the energy group of General Atomics.

.         Eva Tansky Blum, of Pittsburgh, is the Senior Vice President, Director of Community affairs, and chair and President of the PNC foundation, where she makes a significant impact improving the lives of children, their families, and ultimately, their communities. Blum directs the company's philanthropic programs, including PNC Grow Up Great, a ten-year, $100 mill ion program to support quality early childhood education. Blum supports her alma mater, University of Pittsburgh, by serving on the Executive and Institutional Advancement Committees of the Board of Trustees, co-chairs, the University's $2 billion capital campaign and was named Distinguished Alumna in 2007 and Distinguished Law Alumna in 2008.

.         Toi Derricotte, of Pittsburgh, is a professor in the Department of English at the University of Pittsburgh, and has published four books of poems, including Tender, winner of the prestigious Paterson Poetry Prize, and a memoir The Black Notebooks, which received The Anisfield-Wolf Award and was a New York Times notable book of the year. She has won major awards from the Rockefeller Foundation, Guggenheim Foundation, the National Endowment of the Arts, Pushcart Prizes, the Poetry Society of America and the University of Pittsburgh. Toi is co-founder and director of Cave Canem, committed to the discovery and cultivation of new voices in African-American poetry.

.         C. Vivian Stringer, of Princeton, NJ, learned a valuable lesson from her parents growing up in northwestern Pennsylvania: "Work hard, don't look for excuses - you can achieve anything." Stringer is the first coach to take three schools to the NCAA Final Four, the historically black college Cheyney State in 1982, University of Iowa in 1993 and the Rutgers University's Scarlet Knights twice, totaling more than 800 victories. Stringer and the 2007 Rutgers squad captured the nation's respect when faced with the disparaging comments of a radio "shock jock." Stringer was inducted into the coveted Naismith Memorial Basketball Hall of Fame on September 11, 2009.



Cure Alzheimer's Fund's Charles Glabe - Making Strides in Alzheimer's Vaccination Research

In our latest Quarterly Report we highlighted the work of Cure Alzheimer's Fund researcher Dr. Charles Glabe, who is conducting groundbreaking research on vaccinations and immunotherapy. In case you didn't catch the article, here's an excerpt:

Study Led by CAF's Gandy Shows High Protein Diet May Lead to Greater Risk of Alzheimer's

From BioMed Central:

One of the many reasons to pick a low-calorie, low-fat diet rich in vegetables, fruits, and fish is that a host of epidemiological studies have suggested that such a diet may delay the onset or slow the progression of Alzheimer’s disease (AD). Now a study published in BioMed Central’s open access journal Molecular Neurodegeneration tests the effects of several diets, head-to-head, for their effects on AD pathology in a mouse model of the disease. Although the researchers were focused on triggers for brain plaque formation, they also found that, unexpectedly, a high protein diet apparently led to a smaller brain.

A research team from the US, Canada, and the UK tested four differing menus on transgenic mouse model of AD, which express a mutant form of the human amyloid precursor protein (APP). APP’s role in the brain is not fully understood; however it is of great interest to AD researchers because the body uses it to generate the amyloid plaques typical of Alzheimer’s. These mice were fed either (1) a regular diet, (2) a high fat/low carbohydrate custom diet, (3) a high protein/low carb version or (4) a high carbohydrate/low fat option. The researchers then looked at the brain and body weight of the mice, as well as plaque build up and differences in the structure of several brain regions that are involved in the memory defect underlying AD.

Unexpectedly, mice fed a high protein/low carbohydrate diet had brains five percent lighter that all the others, and regions of their hippocampus were less developed. This result was a surprise, and, until researchers test this effect on non-transgenic mice, it is unclear whether the loss of brain mass is associated with AD-type plaque. But some studies in the published literature led the authors to put forward a tentative theory that a high protein diet may leave neurones more vulnerable to AD plaque. Mice on a high fat diet had raised levels of plaque proteins, but this had no effect on plaque burden or brain weight.

Aside from transgenic mice, the pressing question is whether these data have implications for the human brain. “Given the previously re ported association of high protein diet with aging-related neurotoxicity, one wonders whether particular diets, if ingested at particular ages, might increase susceptibility to incidence or progression of AD,” says lead author, Sam Gandy, a professor at The Mount Sinai School of Medicine in New York City and a neurologist at the James J Peters Veterans Affairs Medical Center in the Bronx NY. The only way to know for sure would require prospective randomised double blind clinical diet trials. According to Gandy, “This would be a challenging undertaking but potentially worthwhile, if there is a real chance that the ravages of AD might be slowed or avoided through healthy eating. Such trials will be required if scientists are ever to make specific recommendations about dietary risks for AD.”



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