News

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

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

Summit Success for Alzheimer's Advocate

Alan Arnette, raising funds for Alzheimer's research, successfully completed his first summit as part of The 7 Summits Climb for Alzheimer's. Congratulations Alan! Here is a bit from his most recent dispatch:

The true summit is quite tiny, room for two people with quite a drop-off. But the large summit plateau allowed our entire team of ten to spread out for pictures, videos and push-ups. The view was spectacular. I will post my pictures and a panoramic video when I get home but let me say it was my best summit view ever. This was an emotional moment for me thinking of our goal, my supporters, and my family. I want to dedicate this 1st of the 7 summits to those with early onset Alzheimer's.

The return to High Camp was fast completing a long 12 hour climb followed a nice sleep. With a deteriorating weather forecast, we made a quick trip down from High Camp the next day to Vinson Base Camp - carrying all our tents and climbing gear - to catch the Twin Otter back to Union Glacier. From there the flight back to Punta - eventually. So, the schedule? We understand that the current poor weather pattern will continue for the next 48 hours meaning the earliest we could leave would be Monday, December 13. We are passing the time in somewhat heated 'storm port' shelter during the day and our tents at night - all relative since the sun never sets. As I reflect on the past few weeks, I am grateful to work for your support. Each step on summit day was accompanied by a mantra of "one penny, two penny, three pennies, more" All for research. Climb On! Alan Memories are Everything

Read more of Alan's dispatches>

Pledge to support Cure Alzheimer's Fund and research with every step of Alan's climbs>

CDC Reports Life Expectancy down a bit, but death from Alzheimer’s up 7.5%

The report released on December 9, 2010 by the National Center for health Statistics compares mortality statistics for major diseases between 2007 and 2008 with notes about longer running trends. Alzheimer’s disease remains the #6 cause of death, but jumped 7.5% in the number of deaths between 2007 and 2008. The report also noted that the death rate increased more than 14% from 2003 to 2008.

Several of the leading causes of death saw declines, including heart disease, cancer, stroke, diabetes, homicide and accidents. Infant mortality dropped about 2%. But increases were seen in Alzheimer’s, flue and pneumonia, high blood pressure, suicide and kidney disease, with Alzheimer’s leading the increases.

The full report can be found at http://www.cdc.gov/NCHS.

This disturbing statistic for Alzheimer’s disease should not come as a surprise. Diagnosis and reporting are getting better, and as other causes of death begin to decline, we live longer and are more subject to diseases of aging, such as Alzheimer’s. Plus pure demographics is working against us; the baby boomers are now entering the age where Alzheimer’s becomes apparent.  Approximately 10% of those aged 65 and older have Alzheimer’s; for those 85 and older, the number comes close to half.

While keeping the pressure on to find the causes of and treat these other terrible diseases, we need to regard the Alzheimer’s increase as a clear not-so-early warning that without effective intervention soon, the disease will simply overwhelm us --- our health care systems, our families and an our own and our country’s ability to pay for the care that will be required.

And yet, research budgets at the National Institutes of Health and its National Institute of Aging specifically, continue to erode. We are not facing up to this problem and will pay dearly for it in the not-too-distant future.

Privately funded research can help through focused, strategic pursuit of the real causes of the disease to then accelerate development of effective therapies. But only the government has the resources at sufficient scale to break the back of this disease.

All of us can help by first, contributing to effective, results-oriented private research; and second, by insisting that our elected national officials increase the public’s investment in Alzheimer’s research.

This CDC report should serve as a clarion call to action. If our public officials have either ignored this epidemic until now, or regarded it as “just another problem we have to face”, this report should help order priorities and increase the sense of urgency  around doing all we can to stop this disease.

Raising Money for Research by Climbing in Antarctica

Alan Arnette is in Antarctica climbing Mt. Vinson as part of his 7 Summits Climb for Alzheimer's. Check out his first audio dispatch as he describes his flight in and the pristine snowy landscape of summer near the south pole. It's hard to imagine that it's light all day right now in Antarctica, while at Cure Alzheimer's Fund's main office just outside Boston, it's dark by 5 p.m.

Listen to the dispatch>

Read updates and progress about the Mt. Vinson climb>

Read more about The 7 Summits Climb for Alzheimer's: Memories are Everything>

Alan is attempting to climb the highest peak on each continent as part of a campaign to raise awareness and funds for Alzheimer's research. Every penny donated to Arnette’s quest will go to Cure Alzheimer’s Fund to support research. The cost of the climbs is being covered by the Alzheimer’s Immunotherapy Program of Janssen Alzheimer Immunotherapy and Pfizer Inc. Weather and technology permitting, Alan will be dispatching reports via Twitter and on his blog during his climb. So stay tuned!

Alot of Good Science, Not Enough Funding

Cure Alzheimer's Fund co-founder Phyllis Rappaport hit a key point when interviewed this week by Joe Crankshaw in the Treasure Coast Palm, there isn't enough funding for Alzheimer's research, even though there is a lot of good science that needs to be supported.

Rappaport explains:

We understand so much more about Alzheimer's now then even just four years ago. We have more science then we have money, we have so many avenues to pursue. But this has been an exciting month. The National Neuroscience convention has just ended, and having top scientists discussing our projects and bouncing ideas off each other is exciting.

She also spoke about the devestating impact of Alzheimer's disease and hope for progress with more awareness and funding.

Read the article>