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

Curing Alzheimer's by 2020-TEDMED and Sandra Day O'Connor

Ending the disease by 2020 is a hot topic. The ambitious goal was the focus of Henry McCance and Rudy Tanzi's TEDMED talk yesterday and was a key point in Sandra Day O'Connor's excellent op-ed in the New York Times from earlier in the week. featured a summary of the Tanzi/McCance TEDMED talk:

Dr. Rudolph Tanzi of the Cure Alzheimer's Fund laid out an ambitious goal of finding a cure for the illness by the year 2020. Tanzi and venture capitalist Henry McCance, who helped found the fund in 2004, described the partnership that led to the identification of new genes that seem to play a role in Alzheimer’s disease, genes that are potential targets for new drug therapies.

Read more about TEDMED>

We highly recommend reading The Age of Alzheimer's by Sandra Day O'Connor, Stanley Prusiner and Ken Dychtwald published on Oct. 27, 2010. Just to give you a glimpse of the important message, here's how the piece starts:

OUR government is ignoring what is likely to become the single greatest threat to the health of Americans: Alzheimer’s disease, an illness that is 100 percent incurable and 100 percent fatal. It attacks rich and poor, white-collar and blue, and women and men, without regard to party. A degenerative disease, it steadily robs its victims of memory, judgment and dignity, leaves them unable to care for themselves and destroys their brain and their identity — often depleting their caregivers and families both emotionally and financially.

Starting on Jan. 1, our 79-million-strong baby boom generation will be turning 65 at the rate of one every eight seconds. That means more than 10,000 people per day, or more than four million per year, for the next 19 years facing an increased risk of Alzheimer’s.

Read the NYT Op-ed>

Robert Malenka and Thomas Südhof join Research Consortium

Cure Alzheimer’s Fund is pleased to welcome two new members of the Research Consortium, Dr. Robert C. Malenka and Dr. Thomas C. Südhof. Researchers are invited to serve on the Research Consortium to guide Cure Alzheimer’s Fund-supported work and determine the “roadmap for research” for the most effective and efficient route to slowing, stopping and/or reversing Alzheimer’s disease.

Dr. Robert C. Malenka is the Pritzker Professor of Psychiatry and Behavioral Sciences, director of the Pritzker Laboratory, and co-director of the Stanford Institute for Neuro-Innovation and Translational Neurosciences at the Stanford University School of Medicine. He is a world leader in elucidating the molecular mechanisms by which neural circuits are reorganized by experience. His many contributions over the last 25 years have laid the groundwork for a much more sophisticated understanding of the mechanisms by which neurons communicate and the adaptations in synaptic communication which underlie all forms of normal and pathological behavior. He has been at the forefront of helping to apply the knowledge gained from basic neuroscience research to the treatment and prevention of major neuropsychiatric disorders.

Dr. Südhof is the Avram Goldstein Professor in the School of Medicine at Stanford University. He is also an investigator of the Howard Hughes Medical Institute, a member of the National Academy of Sciences, the Institute of Medicine and the American Academy of Arts and Sciences. Dr. Südhof's research interests focus on the physiological and pathological mechanisms operating on the synapse, in particular on how synapses form, how they transmit signals and how they become abnormal during diseases such as Alzheimer’s disease and autism. His studies have identified key molecules in synapses, such as synaptotagmins, as the calcium sensors for neurotransmitter release, Munc18 as a major fusion protein at the synapse, and neurexins and neuroligins as central trans-synaptic cell adhesion molecules. One of the major current interests in his laboratory is to elucidate the relation of synaptic activity to synapse loss and neurodegeneration in Alzheimer’s disease.


Tanzi and Armour present at White House

The status of research in the United States to find a cure for Alzheimer’s disease was the focus of discussion at a White House-sponsored event on Sept. 21, World Alzheimer’s Day.

Cure Alzheimer’s Fund Research Consortium Chair Dr. Rudolph Tanzi and Tim Armour, president of Cure Alzheimer’s Fund, participated on a scientific panel at the White House event before a select audience of White House senior staff policymakers, leading scientists, advocates and others including Jeff Morby, chairman and co-founder of Cure Alzheimer’s Fund, and Melody Barnes, director of the White House Domestic Policy Council. The topics covered included the current status of biomarker identification for the disease, current thinking about prevention, the strength of the drug pipeline for Alzheimer’s and possible policy initiatives to accelerate progress toward a cure.

Panelists agreed more funding from both the public and private sectors needs to be invested in finding a cure and better treatments; and more aggressive efforts at creating public-private partnerships to provide focus for research efforts is crucial.

All agreed the nation cannot afford to wait, and the development of effective therapies to prevent or stop Alzheimer’s has to be a national priority, backed by a clear strategy and resources to implement it.


Scientific Advisory Board Member Given Lifetime Achievement Award

Marsel Mesulam was recognized for his extraordinary achievements in advancing Alzheimer’s research at the Alzheimer’s Association International Conference on Alzheimer’s Disease 2010 in Honolulu. He is the recipient of the 2010 Bengt Winblad Lifetime Achievement Award. Dr. Mesulam’s research addresses the connectivity of the monkey brain, the organization of human cholinergic pathways, the representation of cognitive functions by large-scale neurocognitive networks and the neurobiology of dementias. Dr. Mesulam’s work on cholinergic pathways has been groundbreaking in understanding Alzheimer’s.

Dr. Mesulam was born in Istanbul in 1945. He received the degrees of bachelor of arts in 1968 and medical doctor in 1972, both from Harvard University. Dr. Mesulam was appointed professor of neurology at Harvard Medical School, where he founded and led the behavioral neurology unit of Boston’s Beth Israel Hospital. In 1994 he was appointed the Dunbar Professor of Neurology and Psychiatry and the director of the multidepartmental Cognitive Neurology and Alzheimer’s Disease Center at Northwestern University’s Feinberg School of Medicine in Chicago. He currently serves on the Cure Alzheimer’s Fund Scientific Advisory Board.

Exploring the Diabetes and Alzheimer’s Link

Researchers hypothesize part of the body’s natural defense against infection may underlie both diabetes and AD.

Cure Alzheimer’s researchers Dr. Rudy Tanzi, chairman of CAF’s Research Consortium and director of the Massachusetts General Genetics and Aging Research Unit, and Dr. Robert Moir from Massachusetts General Hospital were awarded funding from the Helmsley Trust through Cure Alzheimer’s Fund to explore the similarities between the protein amylin in diabetes and its analog in Alzheimer’s, both hallmarks of each disease’s pathology.

“We are deeply grateful for this generous gift from the Leona M. and Harry B. Helmsley Charitable Trust for a $600,000 grant to Cure Alzheimer’s Fund to be paid over two years,” said Tim Armour, president of Cure Alzheimer’s Fund. “This is an exceptional opportunity that is going to allow significant progress into better understanding the twin rising epidemics of diabetes and Alzheimer’s.”

Diabetes mellitus is estimated to affect some 23.6 million Americans today with incidence rates increasing every decade. People most at risk from type II (commonly called mature or late-onset) diabetes are in the same elderly population at risk of Alzheimer’s disease.

A pathological hallmark of both diabetes and Alzheimer’s is the deposition of insoluble proteinaceous deposits called amyloid. Diabetes and Alzheimer’s long have been known to share a broad array of clinical features and a large body of evidence suggests the pathologies of these two disorders are strongly linked. However, as yet no common molecular mechanism has been identified that can explain the long list of epidemiological commonalities between diabetes and Alzheimer’s.

The research, supported by the Helmsley Trust and Cure Alzheimer’s Fund, will focus on the toxic amyloid deposits thought to mediate cellular and tissue degeneration in patients with diabetes and patients with AD and, more specifically, will investigate the activities of the proteins that form diabetic and AD amyloids (for Alzheimer’s this is the Abeta peptide, and for diabetes it is a peptide called amylin).

Drs. Moir and Tanzi recently discovered that the Amyloid-beta protein, a key contributor and acknowledged by most researchers as the “key bad guy” in Alzheimer’s pathology, may have an unsuspected side. The prevailing theory was that Abeta has no function other than as a waste product created by the brain. But research published in the March issue of the journal PLoS One, by Drs. Moir and Tanzi show the protein may be part of the body’s natural defense against infection. This research suggests that Abeta has a very positive function—the peptide may be a natural antibiotic protecting the brain from invading microbes and defending against parasites.

“These data change the way we look at Abeta,” says Dr. Tanzi. “For years, we thought that Abeta was just metabolic garbage produced as a byproduct of other processes within the brain, but new data suggest it is a normal component of the brain’s innate immune system.” Rob Moir adds “Our laboratory has recently shown that Abeta is, in fact, a potent naturally occurring antibiotic. In preliminary experiments we have shown that amylin also appears to be a potent natural antibiotic.”

It appears both proteins may be members of an ancient family of biomolecules called antimicrobial peptides (AMPs) that are the first line of defense against invading organisms. AMPs are the foot soldiers of our innate immune system- an older defense system separate from the antibodies and cells of adaptive immunity.

Notably, while AMPs are critically important for killing invading pathogens, many can also cause collateral damage to host tissue. Aggregation is a key mechanism for the function of AMPs and at least five cause amyloid pathologies. Moir and Tanzi’s findings link, for the first time, the pathologies of diabetes and AD at the molecular level by identifying a common and totally unanticipated antimicrobial function for amylin and Abeta.

These findings suggest that the same or similar site-specific overactive innate immune response to a perceived infection (real or incorrectly identified) may underlie both diabetes and AD. In the brain this response causes Alzheimer’s, when it occurs in the pancreas the result is diabetes.

Confirmation of this hypothesis would prompt a major re-think of the origins of these diseases. In addition, it would identify the pathways of innate immunity as new drug targets for treating, and possibly even preventing diabetes and AD.









Poll Shows Americans favor increase in federal funding for Alzheimer’s research

A new poll shows 88 percent of registered voters believe it is important for Congress to make Alzheimer's a priority despite a growing budget deficit. The poll was conducted by USAgainst Alzheimer's, a Washington, DC group formed specifically to “mobilize America to stop Alzheimer’s by 2020” through aggressive lobbying and support of legislators who support increased funding for Alzheimer’s care and research. Cure Alzheimer’s Fund applauds their efforts and certainly agrees with the need for more resources and a focused strategy at the National level.

Alzheimer’s and Diabetes Link

Alz Forum, the dynamic online scientific knowledge base that reports on the latest Alzheimer's scientific research, has a good article on the recent discovery by Cure Alzheimer’s Fund Researcher Sam Gandy on a link between Alzheimer’s and diabetes, arising from the Alzheimer’s Genome Project which identified new Alzheimer’s gene candidates.

Madolyn Bowman Rogers writes:

Two pernicious disorders of late life, Alzheimer disease and diabetes, may be tied together by a common connection with a pathway that sorts and trafficks proteins such as APP within cells, new research suggests. In the September 29 issue of the Journal of Neuroscience, researchers led by Sam Gandy at Mount Sinai School of Medicine in New York City report that the sorting protein SorCS1 reduces Aβ generation when overexpressed, and conversely is associated with higher levels of Aβ in female mice when underexpressed. SorCS1 has been genetically linked to both diabetes and AD. The convergence of these two diseases on SorCS1 may help explain why having diabetes is a risk factor for contracting Alzheimer’s. The results also suggest a potential new pathway for therapeutic intervention into both disorders.

This paper is important, said Thomas Willnow of the Max-Delbrueck-Center for Molecular Medicine in Berlin, Germany, as it adds pieces to help solve the puzzle of the intracellular trafficking of APP. The data also fit well with previous reports finding that trafficking pathways may be altered in AD, Willnow said. “I think it all adds up and points to a very important aspect of [AD] pathology.”

Read the full article “APP Sorting Protein May Link Alzheimer’s and Diabetes” >

We congratulate Dr. Gandy on this important work and are proud to have helped support it!



New Research Reveals Common Genetic Risk Factor Linking Alzheimer’s Disease and Type 2 Diabetes

Potential for New Therapies to Treat both Diseases

The discovery of a molecular mechanism linking Alzheimer’s disease and Type 2 Diabetes could lead to exciting new drugs to treat both devastating diseases, according to new research published this week in The Journal of Neuroscience.  Researchers found that the gene for a protein called SorCS1, which is linked with Type 2 Diabetes, participates directly in the pathogenesis of Alzheimer’s.

Supported by Cure Alzheimer’s Fund (CAF), the research was led by Dr. Sam Gandy, professor in Alzheimer’s disease research at the Mount Sinai School of Medicine and Dr. Rudy Tanzi, PhD, Harvard University’s Joseph P. and Rose F. Kennedy Professor of Neurology and Director of Genetics and Aging Research Unit. Both are members of the CAF research consortium.  Also part of the team were University of Wisconsin geneticist Alan Attie, PhD, who discovered the linkage of SorCS1 to diabetes in 2007, and Columbia University Alzheimer’s researcher Scott Small, MD.  Rachel Lane, Ph.D., a postdoctoral fellow at Mount Sinai, and Summer Raines, Ph.D., a graduate student at the University of Wisconsin performed the research and shared first authorship.

“Alzheimer’s and Type 2 Diabetes are complex diseases and the risks of both include high cholesterol, obesity and vasculopathy, but these factors are highly interrelated and the challenge has been finding a clear starting point to understand the relationship between the two diseases,” said Gandy. “Our research has revealed a molecular mechanism in the gene SorCS1 that is shared by Alzheimer’s and type 2 diabetes. These findings could open up new doors for more effective treatments for both diseases.”

The research found that the brains of mice genetically deficient in SorCS1, created by Raines and Attie, showed increased levels of amyloid-beta (Abeta), known to play a key role in the onset of Alzheimer’s disease. Meanwhile cells engineered to express high levels of SorCS1 generated low levels of Abeta.

The SorCS1-deficient mice also were found to have abnormally low levels of another protein called Vps35, a profile that Dr. Small linked to Alzheimer’s disease in a 2005 study.  Thus the low SorCS1 might cause levels of Vps35 to go down and lead to the increased formation of Abeta in the mice, and, presumably, Alzheimer’s, in humans.  For the moment, this work provides potential insights and new targets but therapeutic outcomes will require more research.

“Alzheimer’s and Type 2 Diabetes are major causes of illness and death in the elderly and these findings could lead to new drug targets to treat both diseases by increasing levels of SorCS1 or Vps35,” Dr. Tanzi said.  “While further research is needed to find the link between SorCS1 and Vps35, these data will open many new doors.”

“Dr. Gandy and Dr. Tanzi are on the cutting edge of Alzheimer’s research and always take an innovative approach to any challenge they face,” said Tim Armour, president and CEO of Cure Alzheimer’s Fund. “We, at Cure Alzheimer’s Fund, are proud of their work and the hope it offers to the millions of Americans and their families affected by both of these devastating diseases.”

CAF Supported Research by Sam Gandy Reveals Diabetes and Alzheimer’s Link

Cure Alzheimer’s Fund Research Consortium member, Sam Gandy, published research this week in The Journal of Neuroscience linking genes from Alzheimer’s and Type 2 Diabetes. Gandy and other researchers found that the gene for a protein called SorCS1, which is associated with Type 2 Diabetes, participates directly in the pathogenesis of Alzheimer’s.

This work is critically important because it gives new targets for therapy and provides new ways of looking at and understanding both diseases. Watch coverage of this important work on MSN and NBC Nightly News.

Link to video>

Read more about this and how it comes directly from the work of Cure Alzheimer’s Fund’s AGP project conducted by Rudy Tanzi at Mass General Hospital>

Read about this research in Medical News Today>

White House Briefing on Challenge of Alzheimer's

Cure Alzheimer's Fund President, Tim Armour, and Research Consortium Chairman, Rudy Tanzi, were featured in a video from the White House on World Alzheimer's Day. Armour and Tanzi were invited to serve on a special panel to discuss the serious challenge Alzheimer's poses to our nation. Panelists concluded that Alzheimer's is going to have an increasingly devestating effect and all agreed we cannot wait; more must be done to fund research to put an end to this disease as soon as possible.

Read our previous blog on this event>