News

Building Momentum Under the Radar

Breakthrough Research, Strong Fundraising, Mark Fifth Year of Cure Alzheimer’s Fund

Boston – A small nonprofit organization fully dedicated to Alzheimer’s research has quietly been making progress on an ambitious and aggressive research strategy for the development of effective therapies and discovery of an eventual cure for this devastating disease.

Taking a unique venture capital approach to philanthropy, Cure Alzheimer’s Fund (CAF) supports novel Alzheimer’s research that is aggressive, results-oriented, and ‘red-tape’-free. Bucking the recent downturn in charitable donations, the Fund raised a record $3.8 million in 2010 through individuals and federal and foundation grants, plowing all of it directly into research. CAF has raised $18.9 million since its inception at a time when the federal government budget for Alzheimer’s research and education has stagnated.

“Three families committed to wiping out Alzheimer’s decided five years ago that the ‘business-as-usual” model for Alzheimer’s research needed to be accelerated and founded Cure Alzheimer’s Fund,” said Tim Armour, President and CEO of the Fund. “Our network of supporters has grown because the only return the founders expect is a cure and we have made great strides to bring us closer to reaching that goal.”

This year alone CAF-supported research has made significant breakthroughs in better understanding the nature of Alzheimer’s, a key to finding a cure and more effective treatments.  Among that research is the confirmation of a link between Alzheimer’s and Type II diabetes, tied to a molecular mechanism in the gene SorCSI. The research, led by Dr. Sam Gandy, Professor in Alzheimer’s disease Research at the Mount Sinai School of Medicine, could open the door for more effective treatments for both diseases.

Dr. Gandy also developed a new approach for studying brain synapses that has yielded valuable information about the production of Amyloid-Beta oligomers (clumps of the Abeta peptide), which is known to play a key role in the onset of Alzheimer’s disease. Other research led by Dr. Rudy Tanzi, Harvard University Professor of Neurology and Director of Genetics and Aging Research, looked at the theory that Abeta is not entirely a “bad-guy” but in fact is part of the innate immune system.

Dr. Tanzi, who also serves as Chair of the CAF Research Consortium, heads up CAF’s cornerstone project, the Alzheimer’s Genome Project (AGP), which since 2005 has identified over 120 genes that contribute to risk for Alzheimer’s disease. TIME Magazine/CNN named the AGP as one of the top 10 medical breakthroughs of 2008.

“We look for scientists who are doing cutting-edge research and are willing to take a novel or even unconventional approach,” said Armour.

As science technology continues to advance, we believe we are on the cusp of a rare science moment, when intensive research could yield a real breakthrough for an Alzheimer’s cure,” Armour continued.  “With the first of the Baby Boomers turning 65 and experts predicting the number of people diagnosed with Alzheimer’s to skyrocket to 115 million in 2050, that moment can not come soon enough.”

About Cure Alzheimer's Fund

Cure Alzheimer's Fund™ is a 501c3 public charity whose mission is to fund research with the highest probability of slowing, stopping or reversing Alzheimer's disease. Cure Alzheimer’s Fund is characterized by a venture approach to philanthropy that targets funding to specific research objectives. The Fund’s founders underwrite all expenses and overhead, and all contributions go directly to research. The Foundation has no financial or intellectual property interest in the research funded, and will make known the results of all funded research as soon as possible. Cure Alzheimer’s Fund is a national organization with offices in Boston and Pittsburgh. For more information, visit www.curealzfund.org.


Breakthrough Research and Strong Fundraising Mark our Year

A huge thank you to our supporters, researchers and Board of Directors as we celebrate a very successful 2010 at Cure Alzheimer's Fund.

Taking a unique venture capital approach to philanthropy, we support novel Alzheimer’s research that is aggressive, results-oriented, and ‘red-tape’-free. Bucking the recent downturn in charitable donations, we raised a record $3.8 million in 2010 through individuals and federal and foundation grants, plowing all of it directly into research. CAF has raised $18.9 million since its inception at a time when the federal government budget for Alzheimer’s research and education has stagnated.

“Three families committed to wiping out Alzheimer’s decided five years ago that the ‘business-as-usual” model for Alzheimer’s research needed to be accelerated and founded Cure Alzheimer’s Fund,” said Tim Armour, President and CEO of the Fund. “Our network of supporters has grown because the only return the founders expect is a cure and we have made great strides to bring us closer to reaching that goal.”

This year alone CAF-supported research has made significant breakthroughs in better understanding the nature of Alzheimer’s, a key to finding a cure and more effective treatments.

Again, many thanks to all who are helping fund more research so we can get to a cure as quickly as possible. Here's to great progress for 2011.

Read the press release on 2010 success>

NPR Features Interview of Sam Gandy on CAF Funded Research Linking Alzheimer's and Type II Diabetes

National Public Radio's Alan Chartock, from WAMC, hosted Dr. Sam Gandy on his show today. The hour long program focused on Gandy's recent Cure Alzheimer's Fund supported discovery of the link between Alzheimer's and Type II Diabetes. Dr. Gandy, Cure Alzheimer's Fund Research Consortium member is a Mount Sinai Professor of Alzheimer's Disease Research, Professor of Neurology and Psychiatry, and Associate Director of the Mount Sinai Alzheimer's Disease Research Center.

Listen to the show>

Read our blog about this research and how the link between the diseases is helping progress toward a cure for both>

Update from the Board 2010

Dear Friends,
Our focus on funding high-quality, innovative work is fueling great progress in Alzheimer’s research.

It has been an outstanding year at Cure Alzheimer’s Fund. Our strategy of using a business and venture approach for funding research is working. We’ve been recognized in The Wall Street Journal, Time magazine and AARP, featured on NPR and CNN.com and invited to exclusive conferences at the White House, TEDMED and the Milken Institute.

But more importantly, our research is making exceptional progress.

Genetics—In the 104 years after Alois Alzheimer identified the disease, researchers identified only four genes that play a role in the disease. With Cure Alzheimer’s Fund’s support, Rudy Tanzi and his team at Massachusetts General Hospital have identified 120 new candidate genes that affect risk for the disease. More genes mean more understanding of the origins of the disease and a quicker path to effective therapies.

Oligomer summary—CAF-supported research has confirmed that clusters (called “oligomers”) of the Abeta peptide (small protein) form the key toxic element of Alzheimer’s pathology.

Paradigm-shifting discoveries—CAF-funded research recently has shown the Abeta peptide may be a part of the innate immune system in the brain, which strongly suggests effective therapies must modulate or control Abeta production and clearance, not destroy it.

Dimebon—CAF research contributed to an understanding that this recently hailed “wonder drug” for Alzheimer’s really is not.

Drug discovery—Work based on the four Alzheimer’s genes identified almost 25 years ago has led to very promising new compounds that may be much more effective at controlling the production of Abeta, its formulation into oligomers and/or its clearance from the brain.

But the problem is mounting and we need your help to get to a cure.

Alzheimer’s is going to strike half of us who live to be older than 85. As baby boomers move into this age range, Alzheimer’s will bankrupt Medicare and Medicaid, to say nothing of the emotional and economic burden it will bestow on families and caregivers.

To end Alzheimer’s, we think it is imperative to focus private funding on research that is innovative, of the highest quality, speed-driven and results-oriented. Our funded work—upholding these values—can change the research landscape of Alzheimer’s drastically and make great progress toward therapeutic intervention and an end to the disease.

Research is the only way we are going to get to a cure. If you’ve already given to support our research this year, we sincerely thank you. If you have not yet made a contribution to research, we urge you to give generously. Our founders pay all CAF overhead costs, so 100 percent of your dollars goes to research.

Together we can end this terrible disease.

With best regards and wishes for a joyful holiday season.

Henry McCance, Jeff and Jacqui Morby and Phyllis and Jerry Rappaport

MGH Recognizes Cure Alzheimer’s Fund and Tanzi’s Work

Massachusetts General Hospital recognized the significant work of Cure Alzheimer’s Fund and Dr. Rudy Tanzi with three (yes 3!) articles in their most recent newsletter. The first feature highlighted Dr. Tanzi’s work in Alzheimer’s research and the important new theory that Abeta is not entirely a “bad-guy” but in fact is part of the innate immune system. The second article detailed Tim Armour, Cure Alzheimer’s Fund President, and Dr. Tanzi’s participation on a recent White House panel, and the third article recognized the important work that Cure Alzheimer’s is conducting with a special award for the organization’s Founders.

Click here to read the MGH Newsletter >

Passage of National Alzheimer’s Project Act ‘Important Step’ in Battling Disease

Cure Alzheimer’s Fund applauded Congress for passing promising new legislation, the National Alzheimer’s Project Act, praising lawmakers for recognizing the importance of finding a cure for the debilitating disease. The bill would create the National Alzheimer’s Project, which would coordinate government efforts to prevent and treat the disease and create a national strategy for defeating Alzheimer’s disease.

“We commend the Bipartisan Bicameral Congressional Task Force on Alzheimer’s Disease for their action on this legislation,” said Tim Armour, President and CEO of Cure Alzheimer’s Fund. “We especially thank Task Force Co-Chairs Representatives Chris Smith (R-NJ) and Ed Markey (D-MA), and Senators Susan Collins (R-ME) and Mark Warner (D-VA) for their leadership on this bill and commitment to finding a cure for Alzheimer’s. With 5.2 million Americans currently battling this devastating disease and many Baby Boomers reaching the at-risk age, a strategic and coordinated effort to develop more effective treatments and prevention is an important step in battling Alzheimer’s.”

Dedicated to Alzheimer’s research, Cure Alzheimer’s Fund has set forth an ambitious and aggressive national research strategy for the development of effective therapies and discovery of an eventual cure for the disease.

“Finding a cure for Alzheimer’s is a daunting challenge, but with the advances in research and technology over the past decade it is within our reach,” said Armour. “This dedication and commitment by Congress is a encouraging step toward reaching that goal.

“When President Obama signs this bill into law, as is expected, it will mark a significant milestone in the fight against Alzheimer’s disease,” Armour continued.  “It will give hope to the millions of Americans and their families struggling with this devastating disease today.”

A Major Achievement! The Alzheimer's Genome Project

The Alzheimer’s Genome Project™ (AGP) , funded by Cure Alzheimer’s Fund (CAF), is making great scientific progress. This work is providing new understanding of AD pathology and revealing novel genetic information. The more we know about how the disease works, the better the chances are for identifying therapeutic intervention and finding a way to stop it before it starts or interfere once it has started. This is the kind of progress we set out to achieve at CAF and are proud to report on the success of this critical work.

 

Four Years Ago

Cure Alzheimer’s Fund agreed to support the effort to identify all the genes affecting risk for Alzheimer’s disease (AD). Until the mid-1990s, the AD research field had agreed on only four genes as contributing to AD pathology. Three of these were co-discovered by Dr. Rudy Tanzi and his colleagues at Massachusetts General Hospital and Harvard Medical School. All four genes were shown to be involved in the production or clearance of the Abeta protein, which is thought to be at the heart of AD pathology. Most researchers agreed there were many more genes affecting AD pathology, but they were very hard to find and confirm given the limited technology, databases and analytical computer programs at the time. The advent of “gene chips,” the sequencing of the whole human genome in the early 2000s, and major advances in statistical genetics made it now possible to expand upon genetic studies for many complex diseases. The idea was simple in principle—collect samples from families with AD clusters, look at a human genome apparently free of disease and compare it with the genomes of relatives affected by AD. Then focus on those genes or combination of genes that are different in some way in the genomes of those with and without the disease.

This is exactly what Rudy Tanzi and his colleagues proposed to do in late 2005, and they have made great progress. With the help of new technology that provided DNA on computer chips for much more rapid analysis than had been possible, the complete “normal” human genome, and the largest collection of family-based AD DNA in the world, the Tanzi team agreed to a budget of about $3.5 million and a timetable of three years to identify all or most of the remaining genes that affect risk for AD.

Identifying More Than 120 New Alzheimer’s Disease Candidate Genes

The investigation followed two tracks. One was internal to the Tanzi lab, working with the more than 1,000 families and 4,000 individuals from the various AD family-based samples the lab obtained from the National Institute of Mental Health (NIMH), the National Cell Repository for Alzheimer’s Disease (NCRAD), complementary data sets from Australia and Sweden, and samples from MGH/Harvard colleagues Brad Hyman and Deborah Blacker. The second track was to analyze data from all other researchers publishing papers about their identification of AD genes, all of which were collected on a Cure Alzheimer’s Fund-sponsored website called AlzGene (www.alzgene.org). This site not only lists all genes identified by other researchers, but does a “meta analysis” of all the papers’ data to help researchers determine which genes are genuine AD candidate genes and how they rank in terms of genetic power against other such genes. You can see these rankings on the website.

From this intensive, two-track system emerged more than 120 genes newly identified as possible AD genes, or, as the team likes to call them, AD candidate genes. This was done “on time and on budget”—a major scientific and management achievement! Four of the most strongly associated genes were described in a paper published by Dr. Tanzi and colleagues in 2008; this  earned recognition as one of the Top Ten Medical Breakthroughs of 2008 by TIME magazine/CNN.

Understanding How the Candidate Genes Affect Alzheimer’s Pathology

The objective now that an entirely new set of genes influencing AD pathology has been identified has been to determine which of these genes has the greatest effect on the pathology, either in terms of increasing risk OR increasing protection against the disease. Phase 2, in other words, focuses on the highest-priority “hits” as defined by genetic ranking to see what those genes actually do and whether the biological processes in which they are involved might be amenable to modification by drugs. More precisely, in Dr. Tanzi’s words, the objective was to “identify the causal genetic variants and/or mutations responsible for AD.”

For example, gene “A” in its original state may have no relationship to AD pathology at all. However, gene “A” may have developed a mutation over time that now creates a gene that contributes to AD pathology. In Tanzi’s genetic studies, statistically significant association is observed between the gene mutation and the inheritance of AD. Those mutations that show up most often (prevalence) or those that seem to have the most certain or profound effect on brain pathology and dementia (penetrance) are the top priority genes for further investigation. Of these genes, those that provide the greatest opportunities for drug discovery and development then are assigned the highest priority.

Further investigation of these highest-priority genes is called “functional analysis,” because the task now is to determine exactly how the gene affects AD pathology. As researchers look more carefully into these newly identified genes, they are finding that virtually all of them have something to do with either (a) effects on the processing of the APP protein from which Abeta is derived; (b) the production, clearance or in some cases the aggregation of Abeta protein molecules; (c) effects on other AD-related proteins such as Tau; and/or (d) cell death. Another common theme is effects on the brain’s defense system, called the innate immune system. When this system is triggered, Abeta production is enhanced. Dr. Tanzi is finding that many of the new AD candidate genes gauge how robustly the brain’s defense system reacts to such insults as strokes, head bangs, infections and neurotoxins. If one’s genetics leads them to overreact to an insult, the brain produces excessive Abeta. While this may help protect the brain from such things as infection in the short term, too much Abeta in the longer term can cause AD.

Results

Two examples of this functional analysis phase are instructive. One of the genes featured in the TIME/CNN recognition is called ADAM10. The gene has two rare mutations that can cause late-onset (sometimes called “sporadic” onset) AD. Not many people have these mutations, but when they do occur, the individual bearing them has a much higher chance of getting late-onset AD than the general population. ADAM10’s normal activity reduces the level of Abeta production. Both of these mutations impair the activity of ADAM10. The mutations, in other words, contribute to AD pathology by “taking the brakes off” the production of Abeta, which is normally controlled at least in part by the “normal,” nonmutated ADAM10 gene. Enough work and confirmation of this process has been done by Tanzi’s lab, CAF Research Consortium member Dr. Sam Gandy at Mount Sinai Medical School and others to confirm ADAM10 as a genuine Alzheimer’s gene.

The second example is a discovery that may lead to a whole new way of looking at Alzheimer’s pathology and how to prevent it from taking hold or stopping it after it has begun. As mentioned above, Dr. Tanzi identified a number of the newly pegged AD candidate genes as being involved in the innate immune system of the brain. Rob Moir of Massachusetts General Hospital/Harvard Medical School, working in Dr. Tanzi’s unit, found that Abeta may play a role in the innate immune system as an anti-microbial peptide that can fight infection. That means that Abeta may in fact have a positive, constructive role to play in the brain, but becomes toxic and leads to AD when it accumulates in excessive amounts.

What follows from both these examples is that rather than trying to extinguish completely the production of Abeta as some drugs have tried to do, or trying to limit its presence in the brain to negligible levels as others have tried, the more successful approach may be to modulate the process of production and clearance to maintain the “appropriate” level of Abeta in the brain to allow it to do its more positive and helpful work, but not to accumulate to excessive levels. Along these lines, Cure Alzheimer’s Fund is supporting a drug discovery program in Dr. Tanzi’s lab and Dr. Steven Wagner’s lab at the University of California, San Diego to develop “gamma secretase modulators,” drugs that will safely lower Abeta levels in the brain without wiping them out.

These and other discoveries will come more rapidly now that the whole Alzheimer’s genome has been mapped or “sequenced” and if the resources are available to follow up and confirm the strong AD candidate genes and their role in Alzheimer’s pathology. The more we know about them and how they do their work, the more able we are to stop them from starting AD pathology and to slow or stop it once it starts.

Leveraging Cure Alzheimer’s Fund support leads to impressive RO1 grants

At Cure Alzheimer’s Fund, one of our successful strategies is to fund research that is innovative and based on high-quality science yet deemed risky by traditional funding sources. Our entrepreneurial approach and ability to provide funds in a quick and efficient manner allows us to fund potentially groundbreaking work that otherwise might sit unpursued.

This approach is making a dramatic difference. In 2009, we reported two very successful examples of this type of leveraging by our funded researchers Robert Moir and Giuseppina Tesco. Moir’s concept that the Abeta peptide is an antimicrobial peptide, and part of the innate immune system, initially was funded by Cure Alzheimer’s Fund, and this work led to an RO1 grant, the original and histroically oldest grant mechanism from the National Institutes of Health. Cure Alzheimer’s Fund supported Tesco’s pilot studies exploring the relationship between traumatic brain injury and Alzheimer’s, which allowed her to secure an RO1 grant.

And 2010 has brought even more success, with four more leveraging examples and others in the pipeline.

Charlie Glabe from University of California, Irvine, used his CAF project on anti-oligomer monoclonal antibodies as the preliminary data to support a new NIH RO1 award of $1 million over 5 years.  He used some of the antibodies he made in the CAF project to show that different types of amyloid oligomers exist and that they warrant further study to determine their role in AD. His RO1 grant will explore the structural heterogeneity of amyloid aggregates and the relationships of this conformational variation to the toxicity or pathogenic activities of amyloid oligomers.

David Holtzman at Washington University, St. Louis, explains his successful use of CAF funds:

“One of my CAF grants enabled me to gather preliminary data and publish papers that facilitated a grant application to the Ellison Medical Foundation, and within the last year, I applied for the Ellison Foundation Senior Scholar Award. The grant is related to my work on how synaptic activity regulates the Abeta peptide and the sleep/wake cycle. My application was successful and I was awarded a grant which started in October for $600,000 in direct costs over four years.”

Virginia Lee and colleagues at the University of Pennsylvania proposed an innovative way to significantly reduce Abeta levels and plaque deposition in an established mouse model of Alzheimer’s disease with their “Brain-Penetrant Thromboxane Antagonists for Alzheimer's Disease Therapy” grant from Cure Alzheimer’s Fund. Their approach involved disrupting a particular biochemical process in which an omega 6 fatty acid that activates the thromboxane (TP) neuronal receptor in the brain stimulates excess Abeta production. Antagonists (drugs or compounds that bind to a receptor) previously used for this purpose did not successfully bridge the blood brain barrier and therefore proved ineffective. New technology suggested that novel compounds to intervene in this process also might be able to penetrate the blood brain barrier with minimal-to-no toxicity or other negative effects. The project showed considerable progress in the synthesis and evaluation of a number of TP receptor antagonists that are brain-penetrant.

This “proof of concept” work enabled the team to secure much greater funding, a five-year RO1 grant totaling more than $2.3 million from the federal government for further development of this high-potential therapeutic approach. Continuation of this work is ongoing in the drug discovery program in their Center for Neurodegenerative Disease Research.

Sam Gandy also parlayed his Oligomer Collaborative funding from Cure Alzheimer’s into a three-year Department of Veterans Affairs grant.

This type of support is a big win all around. Cure Alzheimer’s Fund grants are providing seed capital to researchers to prove a concept and then leverage start-up funding into much larger government and private grants. Stay tuned for updates and more examples.

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At Cure Alzheimer’s Fund, one of our successful strategies is to fund research that is innovative and based on high-quality science yet deemed risky by traditional funding sources. Our entrepreneurial approach and ability to provide funds in a quick and efficient manner allows us to fund potentially groundbreaking work that otherwise might sit unpursued.

This approach is making a dramatic difference. In 2009, we reported two very successful examples of this type of leveraging by our funded researchers Robert Moir and Giuseppina Tesco. Moir’s concept that the Abeta peptide is an antimicrobial peptide, and part of the innate immune system, initially was funded by Cure Alzheimer’s Fund, and this work led to an RO1 grant from the National Institutes of Health. Cure Alzheimer’s Fund supported Tesco’s pilot studies exploring the relationship between traumatic brain injury and Alzheimer’s, which allowed her to secure an RO1 grant.

And 2010 has brought even more success, with four more leveraging examples and others in the pipeline.

Charlie Glabe from University of California, Irvine, used his CAF project on anti-oligomer monoclonal antibodies as the preliminary data to support a new NIH RO1 award of $1 million over 5 years. He used some of the antibodies he made in the CAF project to show that different types of amyloid oligomers exist and that they warrant further study to determine their role in AD. His RO1 grant will explore the structural heterogeneity of amyloid aggregates and the relationships of this conformational variation to the toxicity or pathogenic activities of amyloid oligomers.

David Holtzman at Washington University, St. Louis, explains his successful use of CAF funds:

“One of my CAF grants enabled me to gather preliminary data and publish papers that facilitated a grant application to the Ellison Medical Foundation, and within the last year, I applied for the Ellison Foundation Senior Scholar Award. The grant is related to my work on how synaptic activity regulates the Abeta peptide and the sleep/wake cycle. My application was successful and I was awarded a grant which started in October for $600,000 in direct costs over four years.”

Virginia Lee and colleagues at the University of Pennsylvania proposed an innovative way to significantly reduce Abeta levels and plaque deposition in an established mouse model of Alzheimer’s disease with their “Brain-Penetrant Thromboxane Antagonists for Alzheimer's Disease Therapy” grant from Cure Alzheimer’s Fund. Their approach involved disrupting a particular biochemical process in which an omega 6 fatty acid that activates the thromboxane (TP) neuronal receptor in the brain stimulates excess Abeta production. Antagonists (drugs or compounds that bind to a receptor) previously used for this purpose did not successfully bridge the blood brain barrier and therefore proved ineffective. New technology suggested that novel compounds to intervene in this process also might be able to penetrate the blood brain barrier with minimal-to-no toxicity or other negative effects. The project showed considerable progress in the synthesis and evaluation of a number of TP receptor antagonists that are brain-penetrant.

This “proof of concept” work enabled the team to secure much greater funding, a five-year RO1 grant totaling more than $2.3

At Cure Alzheimer’s Fund, one of our successful strategies is to fund research that is innovative and based on high-quality science yet deemed risky by traditional funding sources. Our entrepreneurial approach and ability to provide funds in a quick and efficient manner allows us to fund potentially groundbreaking work that otherwise might sit unpursued.

 

This approach is making a dramatic difference. In 2009, we reported two very successful examples of this type of leveraging by our funded researchers Robert Moir and Giuseppina Tesco. Moir’s concept that the Abeta peptide is an antimicrobial peptide, and part of the innate immune system, initially was funded by Cure Alzheimer’s Fund, and this work led to an RO1 grant from the National Institutes of Health. Cure Alzheimer’s Fund supported Tesco’s pilot studies exploring the relationship between traumatic brain injury and Alzheimer’s, which allowed her to secure an RO1 grant.

 

And 2010 has brought even more success, with four more leveraging examples and others in the pipeline.

 

Charlie Glabe from University of California, Irvine, used his CAF project on anti-oligomer monoclonal antibodies as the preliminary data to support a new NIH RO1 award of $1 million over 5 years.  He used some of the antibodies he made in the CAF project to show that different types of amyloid oligomers exist and that they warrant further study to determine their role in AD. His RO1 grant will explore the structural heterogeneity of amyloid aggregates and the relationships of this conformational variation to the toxicity or pathogenic activities of amyloid oligomers.

 

David Holtzman at Washington University, St. Louis, explains his successful use of CAF funds:

 

“One of my CAF grants enabled me to gather preliminary data and publish papers that facilitated a grant application to the Ellison Medical Foundation, and within the last year, I applied for the Ellison Foundation Senior Scholar Award. The grant is related to my work on how synaptic activity regulates the Abeta peptide and the sleep/wake cycle. My application was successful and I was awarded a grant which started in October for $600,000 in direct costs over four years.”

 

Virginia Lee and colleagues at the University of Pennsylvania proposed an innovative way to significantly reduce Abeta levels and plaque deposition in an established mouse model of Alzheimer’s disease with their “Brain-Penetrant Thromboxane Antagonists for Alzheimer's Disease Therapy” grant from Cure Alzheimer’s Fund. Their approach involved disrupting a particular biochemical process in which an omega 6 fatty acid that activates the thromboxane (TP) neuronal receptor in the brain stimulates excess Abeta production. Antagonists (drugs or compounds that bind to a receptor) previously used for this purpose did not successfully bridge the blood brain barrier and therefore proved ineffective. New technology suggested that novel compounds to intervene in this process also might be able to penetrate the blood brain barrier with minimal-to-no toxicity or other negative effects. The project showed considerable progress in the synthesis and evaluation of a number of TP receptor antagonists that are brain-penetrant.

 

This “proof of concept” work enabled the team to secure much greater funding, a five-year RO1 grant totaling more than $2.3 million from the federal government for further development of this high-potential therapeutic approach. Continuation of this work is ongoing in the drug discovery program in their Center for Neurodegenerative Disease Research.

 

Sam Gandy also parlayed his Oligomer Collaborative funding from Cure Alzheimer’s into a three-year Department of Veterans Affairs grant.

 

This type of support is a big win all around. Cure Alzheimer’s Fund grants are providing seed capital to researchers to prove a concept and then leverage start-up funding into much larger government and private grants. Stay tuned for updates and more examples.

million from the federal government for further development of this high-potential therapeutic approach. Continuation of this work is ongoing in the drug discovery program in their Center for Neurodegenerative Disease Research.

Sam Gandy also parlayed his Oligomer Collaborative funding from Cure Alzheimer’s into a three-year Department of Veterans Affairs grant.

This type of support is a big win all around. Cure Alzheimer’s Fund grants are providing seed capital to researchers to prove a concept and then leverage start-up funding into much larger government and private grants. Stay tuned for updates and more examples.

Board Update 2010: Our work is fueling progress

Our focus on funding high-quality, innovative work is fueling progress in Alzheimer’s research

Dear Friends,

It has been an outstanding year at Cure Alzheimer’s Fund(CAF). Our strategy of using a business and venture approach for funding research is working. We’ve been recognized in The Wall Street Journal, Time magazine and AARP, featured on NPR and CNN.com and invited to exclusive conferences at the White House, TEDMED and the Milken Institute.

NY Times article highlights Abeta research of Cure Alzheimer Fund Researchers

Three members of Cure Alzheimer's Fund Research Consortium - Dr. David Holtzman, Dr. Robert Malinow and Dr. Sam Gandy - are featured in a New York Times article highlighting their groundbreaking work on amyloid beta protein and its role in Alzheimer's. Veteran reporter Gina Kolata discusses how their important research is part of "a wave of unexpected findings" leading to new insights about the disease and potential new drug targets to attack Alzheimer's.

Dr. Holtzman put it best in the article how these new findings are offering real hope to the millions of people living with this devastating disease and their families. “We have a richer view of the genesis of Alzheimer’s disease as well as new directions for research, prevention and treatment.”

Read the full article here:
http://www.nytimes.com/2010/12/14/health/14alzheimers.html?pagewanted=1&_r=1&ref=science