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

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.”



Media Contact

Charlotte Webber
Press Office, BioMed Central
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Lifetime Achievement Award to Virginia Lee, Ph.D.

Virginia M.-Y. Lee, Ph.D.The Khalid Iqbal Lifetime Achievement Award for 2009 was bestowed upon Cure Alzheimer’s Fund Research Consortium member and funded researcher Virginia M.-Y. Lee, Ph.D.

Khalid Iqbal, Ph.D., was one of the founders of the International Conference for Alzheimer’s Disease in 1988. A Lifetime Achievement Award named in his honor is given to an outstanding scientist who has dedicated his or her career to helping millions around the world through research.

Dr. Lee is director of the University of Pennsylvania’s Center for Neurodegenerative Disease Research. Her research focus includes determining the genesis and roles of various normal and abnormal brain proteins (amyloid, tau, etc.) thought to be the keys to the cause and progression of numerous brain diseases, including Alzheimer’s.

Running to Fight Alzheimer's

Maria Pugliese Running to Fight Alzheimer'sMaria Pugliese is running the Buenos Aires marathon October 11 in support of Cure Alzheimer’s Fund.

“My grandmother suffers from the disease and every day is a challenge for her and those around her,” Maria says. “As genetics plays a key role in the disease, it is likely that this will continue to affect my family. I want to do everything possible to try and advance the research so fewer and fewer people suffer.”

Vaccination and Immunotherapy for Alzheimer’s Disease

Vaccination against amyloid is a promising approach for the development of Alzheimer’s disease (AD) therapeutics. Approximately half of the investigational new therapeutics in human clinical trials for AD are active or passive immunotherapeutics.

Active vaccination involves the injection of an antigen and relies on the production of antibodies in the vaccinated patient. Four human clinical trials of active vaccination currently are under way. Passive immunization is also a promising strategy that involves the production of antibodies outside of the patient and injection of these antibodies. There are currently 12 clinical trials of passive immunization. You can check for Alzheimer therapeutics in human clinical trials by visiting and searching for key words “Alzheimer’s and immunotherapy.”

Thinking out of the box

The development of vaccinations as a strategy for treating or preventing Alzheimer’s is an example of thinking out of the box. Vaccinations commonly are associated with infectious diseases, like influenza, small pox and polio, which appear to have little in common with neurodegenerative diseases, like Alzheimer’s. Moreover, the brain is an immunoprivileged site with little access to antibodies, so it seems unlikely antibodies would be protective in the brain.

Researchers were pleasantly surprised when Dale Schenk and co-workers at Elan Inc. reported that vaccination of transgenic mouse models of AD against the amyloid Aß peptide prevented amyloid deposition in young animals and removed pre-existing amyloid deposits in older animals. Subsequent work showed that immunization against Aß prevented or reversed many other pathological features and prevented cognitive dysfunction in transgenic mice and non-human primates. This vaccine (Elan AN1792) was tested in human clinical trials, where it showed similar beneficial effects of removing amyloid deposits and slowing cognitive decline in patients with significant levels of anti-Aß antibodies, but the clinical trial was halted because 6 percent of the patients developed meningoencephalitis, an inflammatory side effect.

Second-generation vaccines and passive immunization

To circumvent the unwanted inflammatory side effects, second-generation active vaccines have been developed and passive immunization strategies have been explored. The second-generation vaccines use small pieces of the amyloid Aß sequence to avoid activating the T-cells responsible for meningoencephalitis, while passive immunization bypasses the human immune response by directly supplying antibodies. These newer strategies have shown the same beneficial effects in transgenic mice and passive immunization has shown some promise in a subset of patients in human trials, but they have raised new questions about their effectiveness and potential new side effects. Elan/Wyeth reported preliminary results from clinical trials of their monoclonal antibody, Bapineuzimab, that demonstrated only a small benefit in a subgroup of patients who lack the apoE4 genotype. They also failed to observe an improved benefit with an increased dose of antibody and reported side effects, like a buildup of fluid in the brain. Results of active vaccination human clinical trials with second-generation vaccines remain to be reported.

Third-generation vaccines and antibodies: Thinking perpendicular to the box

Both second-generation vaccines and antibodies suffer from a common problem. They both target linear amino acid sequences found in normal human proteins (the amyloid precursor protein) and in the amyloid deposits themselves. Making antibodies against normal human proteins can cause autoimmune side effects, in which the immune system is attacking normal human cells in addition to the Alzheimer’s pathology. Fortunately, it is difficult to make antibodies against self-proteins because of immune suppression of auto antibodies. Third-generation vaccines seek to overcome these problems of autoimmune side effects and autoimmune suppression by using antibodies that target structures specific to the amyloid aggregates and that do not react with normal human proteins.

Cure Alzheimer’s Fund has been supporting two projects that seek to develop third-generation immunotherapeutics. Dr. Charles Glabe’s laboratory is developing active vaccines and monoclonal antibodies that recognize conformations of the amyloid peptide that only occur in the pathological amyloid oligomer aggregates, while Dr. Rob Moir’s lab is working on cross-linked amyloid peptides (CAPs) that are only found in disease-related aggregates. Dr. Glabe’s strategy relies on the fact that when the Aß peptide aggregates into ß-sheet oligomers, it creates new antibody recognition sites, known as epitopes, that are not found on native proteins. The surprising finding is that these oligomer-specific antibodies recognize amyloid oligomers from other diseases that involve amyloids formed from sequences unrelated to Aß. This means the same antibodies also may be effective for other amyloid-related neurodegenerative diseases, like Parkinson’s disease.

The explanation for why the antibodies are specific for amyloid oligomers that involve several individual peptide strands arranged in a sheet and yet recognize these sheets when they are formed from other amino acid sequences is simple and elegant (Figure 1). It is now known that most pathological amyloids aggregate into simple and very regular structures where the peptide strands are arranged in parallel and where the amino acid sequence is in exact register. This is like a sheet of paper upon which the same sentence is written on each line. The individual amino acids line up and down the sheet in homogeneous tracts, known as “steric zippers.” The steric zippers do not occur in normal protein structures and the oligomer-specific antibodies are thought to recognize these steric zipper patterns on the surface of the sheets. Since all proteins are made up using the same 20 amino acids, any sequence in this parallel, in-register structure gives rise to the same steric zippers regardless of the linear sequence, which can explain why the antibodies recognize the oligomers formed by different proteins.

Dr. Moir’s group is working on CAPs, where Aß is cross-linked by oxidation of a tyrosine residue at position 10 of the peptides’ sequence. Aß is oxidized after it is produced from the amyloid precursor protein as a consequence of the abnormally high level of oxidative activity in a brain with AD and the peptides’ propensity to bind redox active metals. Excessive CAPs generation is associated with the disease state and is not a normal feature of Aß biology. The cross-linking at tyrosine 10 that gives rise to CAPs may serve to align the peptides in a parallel, in-register fashion and promote the generation of still-larger oligomeric aggregates that display steric zippers on their surface.

Dr. Moir and Dr. Rudy Tanzi’s labs found that natural antibodies to CAPs are reduced in the blood of patients with AD. More recently, evidence published by Tony Weiss-Coray’s group at Stanford University supports the idea that antibodies that recognize steric zippers and CAPs may be important for protecting against Alzheimer’s disease. The levels of these antibodies that target the zippers and CAPs were among the highest in young, normal humans; levels dropped with aging and with AD. Furthermore, the results of a recent study supported by Baxter Biosciences of patients that received human antibodies purified from normal individuals (IVIg) reported that antibody treatment reduced the risk of being diagnosed with AD by 42 percent over the five-year study period. This is one of the most remarkable reports of prevention of AD by any therapy. Although the normal human antibodies that target amyloid primarily recognize the steric zippers and CAPs, these antibodies are present at relatively low levels. It is reasonable to imagine that an even greater protective effect might be achieved by boosting the levels of these protective antibodies by either active vaccination or passive immunization.

Figure 1

Figure 1 shows how the same steric zipper patterns are formed on parallel, in-register oligomers from completely different sequences. A segment of the Aß sequences is shown in the upper left corner and a random sequence is shown in the upper right. Each amino acid is designated by a capital letter. Typical antibodies recognize the linear sequence (from left to right) indicated in the horizontal boxes, which is unique to each sequence. When the peptides aggregate to form pathological oligomers, they line up in a parallel, in-register fashion, shown below. This gives rise to steric zippers that run up and down the sheet perpendicular to the sequence, shown in vertical boxes. Aggregation-dependent, disease-specific antibodies recognize the steric zippers from many different amyloid sequences. Zippers from F and V amino acids are shown in boxes, but there are potentially 20 different zippers; one for each of the 20 amino acids.

The fact that a completely random sequence can form the same type of steric zipper as is found in Aß amyloid in Alzheimer’s disease means we can use a non-human, random peptide sequence as a vaccine to produce a protective immune response that has a very low potential for autoimmune side effects. Vaccines based on non-human peptides, like diphtheria and pertussis toxin, are so safe they routinely are given to infants. There is no reason to expect that a vaccine for AD that targets the disease-specific steric zippers wouldn’t be as safe and free of side effects. A goal of the research funded by Cure Alzheimer’s Fund is to do the preclinical investigations that are a necessary prelude to getting these third-generation vaccines and monoclonal antibodies that target disease-specific epitopes into human clinical trials.

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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