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

Help us win $250,000 for Alzheimer’s research -- Vote today!

By Tim Armour

Every 70 seconds, another American is diagnosed with Alzheimer’s -- that’s over 5 million Americans suffering from this devastating disease each and every day.

But today, we have the unique opportunity to perform one simple act that could make a big difference in the fight against Alzheimer’s.

Through the Pepsi Refresh Project, Cure Alzheimer’s Fund has the chance to win a $250,000 grant that would fund the groundbreaking research that will help us find a cure to this destructive disease.

But we need your help to make this funding a reality!

Just visit and click “vote for this idea.” Then register with Pepsi Refresh by entering your email and password so you can easily vote every day!

We started Cure Alzheimer's Fund because we want to find a cure now. We’re the only organization with a roadmap to a cure -- we just need the funding to make it a reality. The Pepsi Refresh grant can make a big difference, bringing us that much closer to a cure.

What you do right now really matters. Please send the link to everyone you know and ask them to join you in voting for Cure Alzheimer’s Fund. It’s a very small step, but one that could mean the world of difference to Alzheimer’s sufferers everywhere.

Voting runs now through April 30th, and remember, you can vote once a day so vote early and vote often!

The Good News

By Tim Armour

From the new findings about oligomers, many supported by Cure Alzheimer’s Fund, we know a lot more about the toxicity of the Abeta42 oligomers and how that affects the neural synapses. None of these first or second generation drugs were aimed at stopping Abeta 42 aggregation or oligomerization; nor were any of them directed toward protecting the neural synapses. They were more directed toward stopping Abeta production altogether through modifying or eliminating steps in the production process.

Furthermore, from new and potentially paradigm-breaking research also sponsored by Cure Alzheimer’s Fund, we now know that Abeta42 may be an integral part of the innate immune system. In other words, it is actually good for fighting off bugs in our system, particularly in the brain, and to develop drugs to stop its production completely or dramatically reduce it would be a big mistake.

Third, Cure Alzheimer’s Fund is supporting new research on more promising approaches to the regulation of Abeta. One of these tracks is the exploration of a whole new class of “gamma secretase modulators” which are safe and more potent that those used in Flurizan or other failed drug tests. A second is experimentation with drugs that specifically target one step of the cholesterol pathway, acyl-coenzyme A: cholesterol acyltransferase (ACAT) inhibitors, reducing generation of toxic Aβ peptide in cells and in an animal model of AD. And finally, other research being funded by Cure Alzheimer’s Fund is screening all approved (and therefore safe) drugs in the entire human pharmacopeia to see which ones lower Abeta levels.

Were those first and second generation drugs “failures?” If measured by their ability to stop the disease or provide immediate relief to patients -- then yes -- and that is clearly what is most important. However, in their failure, they have helped to correct the direction along the “Abeta trail” and help us focus on more effective therapeutic approaches.

Where do we go from here? One conclusion is to keep following the Abeta trail. It is increasingly clear that it is the seminal actor in Alzheimer’s pathology.

Second, primary therapeutic targets based on this information should be focused on at least three approaches:

  • Continue to find ways to “modulate” the production of Abeta to prevent over-production, but allow that amount that is actually helpful or protective to continue to be made and safely deployed;
  • Find ways to prevent the “oligomerization” of the Abeta42 peptide in its most toxic forms.
  • Continue to explore the Abeta/neural synapse relationship to maximize Abeta’s potential protective capability and reduce its toxicity.

This will require heeding the lessons from what we are learning from genetics, now having identified over 100 candidate Alzheimer’s genes for more study about how they affect risk for the disease, what the first and second generation drugs have taught us, and aggressive exploration of newer perspectives on the role of Abeta42 and how it can be modulated safely for effective reduction or elimination of risk for Alzheimer’s.

It is a challenging task that will require significantly increased resources. But the way forward is clear; follow the Abeta trail.


The Success Stories of Tomorrow

By Tim Armour

Yesterday I discussed the scientific community’s profound disappointment in the failure of three different, high-profile Alzheimer’s drugs. But despite their inabilities to get at the root of this disease, they have played an important role in what will likely be the success stories of tomorrow.

First, all of these drugs addressed what most researchers believe is the key “bad guy” in Alzheimer’s disease pathology --- the small protein (peptide) Abeta, and particularly it’s genetic variant, Abeta42 (that means there are 42 molecules of the Abeta variant in this species instead of the more frequent 40 or other conformations). The Abeta trail is a long and winding one which first pointed to Abeta42 as the substance which formed the plaques in the brain that somehow extinguished brain cell communication. Recently, the Alzheimer’s research field has moved to a more sophisticated understanding of how Abeta42 does its work. It is now increasingly thought to be toxic only or primarily in its aggregated, clumped or “oligomer” form. These oligomers are now seen to be forming at or near the neurons in the brain responsible for the neural communication that enables acquisition of new information and creation of memory.

The science of all of this is complicated and rapidly evolving, but the essence is that the focus of the cause of the disease has moved for the most part from the plaques to the formulation of the Abeta peptide itself and its coalescing into the more toxic oligomers.

One great challenge to the rapid evolution of the understanding of the causes of the disease is the assault on the “Abeta” thesis because of the failure of these drugs to stop the disease. If their target was the control or elimination of Abeta42 and they failed, the reasoning goes, maybe Abeta42 is the wrong target.

Not so fast.

1). The early drugs and this second “failed” generation have focused on trying to stop Abeta42 from forming in the first place. Flurizan, for example, was designed to block Abeta42 production by modulating an enzyme important to Abeta42 creation (“gamma secretase”). The drug failed because it was not potent enough to affect change in Abeta levels; stronger doses delivered to human patients created fatal side effects. That means that the theory of the “mechanism of action” is probably not wrong, but this particular drug compound and its near relatives failed to achieve the appropriate risk/effectiveness balance.

2). Bapineuzumab was based on Abeta immunotherapy (passive immunization) in which antibodies targeting Abeta are injected intravenously into AD patients. While initial trial data looked promising, more recent trials showed that, once again, high enough does of the drug to be effective caused dangerous side effects for patients. A further complication is that the drug appeared to be slightly more effective in the group of patients which do NOT carry the best known and most prevalent Alzheimer’s gene, APOE4. The hurdles to re-balancing this particular family of compounds will prove to be a great challenge for Johnson and Johnson’s Alzheimer’s unit.

3). Finally, Dimebon. A strange story indeed, and a heartbreaking one for patients and their families who read about the promise of this “wonder drug.” While the Dimebon “method of action” against Alzheimer’s pathology is not yet apparent, what is clear is that based on the rigorous (but hopeful!) US trials, the drug does not work. It is safe, but completely ineffective. Some who know this story more intimately suspect that the original Russian data was misleading; others simply don’t know what to make of the disparity. In any case, there appears to be little or no hope for this drug as an effective therapy against Alzheimer’s disease.

What does all this tell us? Aside from dashed hopes and ruined companies, what it does NOT tell us is that the Abeta trail is a wild goose chase. Not at all.

So where does this leave us? Stay tuned tomorrow for the good news!

Why Don't the Drugs Work

By Tim Armour

A spate of headlines recently dimmed hopes for a wonder drug to fight Alzheimer’s disease. We know that the existing drugs used to treat Alzheimer’s patients including Aircept, Numenda, and others provide only modest symptomatic relief but do not treat the root pathology of the disease.

In a series of posts this week, we’ll look at three new drugs which attempted to get at the causes of the disease but failed. We’ll look at the “bad news,” comment on why they failed and then look at what’s in the pipeline signaling better news.

1). The first high profile failure was Flurizan (tarenflurbil) by Myriad Genetics. A June 30, 2008 report by Myriad CEO Peter Meldrum concluded, “We are disappointed that Flurizan failed to achieve significance and we will now discontinue development of this compound.” Womp went Myriad’s stock and the hopes of millions as a result of this $60 million “failure.”

2). The second is the disappointing results of trials for bapineuzumab (acronym for “Beta Amyloid Peptide (I) Neutrali Z ing (U) M onoclonal Antibody) by pharmaceutical partners Elan and Wyeth. The companies tried several variations of doses of this drug, but experienced safety issues at the higher, more effective doses because of the presence of vasogenic edema in some of the study’s patients. “Bap’s” development has now been taken over by Johnson and Johnson’s Janssen Alzheimer’s Immunotherapy unit which announced, on March 17th, an extension of current trials with no announcement about results of those trials until 2012.

3). Third is the very recent spectacular rise and fall of Dimebon, a drug developed in Russia as an antihistamine and brought to the US after extensive review of the Russian trials as an Alzheimer’s drug. Initial data was, in essence, “too good to be true” in its apparent ability to lower Abeta in the brain and cause a decrease in Alzheimer’s symptoms. Subsequent trials in the US by the drug’s US licensee, Medivation and its partner Pfizer, could not replicate this “too good to be true” data. In fact, US-based trials, known as CONNECTION, showed no benefit whatsoever. The day the results of these US trials were announced, March 3, 2010, Medivation lost 70% of its value.

We all know that drug making is a high risk business. The pharmaceutical companies tell us this all the time, supporting what many people regard as very high prices on the fewer successful drugs in order to support the risk-taking. Some of this is absolutely true; but without getting into the economics of this issue here, let’s look at the science.

Why did these drugs fail, and in their failure can they help us improve on the next generation of therapies?

Stay tuned for the answers to those questions tomorrow, here on the blog.

Dr. Tanzi Presents "State of the Art" Lecture at the Prestigious International Geneva/Springfield Symposium on Advances in Alzheimer's Therapy

The researchers who support the Cure Alzheimer Fund always impress us!

Dr. Rudy Tanzi, Chair of the Cure Alzheimer’s Fund Research Consortium, director of the Aging and Genetics Unit at Massachusetts General Hospital and Kennedy Professor of Neurology at Harvard Medical School, was asked to deliver a “State of the Art” lecture on Friday, March 26, at the 11th International Geneva/Springfield Symposium on Advances in Alzheimer’s Therapy.

The bi-annual event distinguishes itself from other scientific meetings by “focusing entirely on the pharmacological therapy of Alzheimer’s Disease with particular emphasis on the discovery of new drugs” and the fact that it is organized by a European entity, University of Geneva Medical School, and a university in the United States, Southern Illinois University School of Medicine. Tanzi spoke about “Novel Alzheimer disease genes and emerging biological pathways”, and building on his laboratory’s identification of over 100 candidate Alzheimer’s genes, funded by Cure Alzheimer’s Fund. The conference runs for four days and brings together leading Alzheimer’s researchers from around the world.

Alzheimer’s as a Barrier to Retirement

We’ve talked about Alzheimer’s disease from almost every possible angle here on the blog, but according to MarketWatch, there is one major implication of diagnosis that we haven’t discussed -- Alzheimer’s as a barrier to retirement.

Robert Powell’s article stresses that while most Americans worry about tax rates and 401Ks when preparing for retirement, there is a clear elephant in the room -- Alzheimer’s.

5.3 million Americans currently suffer from Alzheimer’s, but most families fail to prepare for the disease. And what is perhaps most alarming is that the number of cases is expected to skyrocket to 19 million by 2050.

While I won’t delve into the details of retirement planning here (you can learn more about how to prepare for retirement with Alzheimer’s by checking out Powell’s article), this is just one more reason why we must prepare for what many have called the “silver tsunami.” Life expectancy rates in this country are at an all-time high and with advanced age comes the increased threat of Alzheimer’s.

Alzheimer’s is hurting our nation’s families and bankrupting our country’s health care system. Isn’t it time for our federal government to invest in research and finally put an end to this devastating disease?

CAF Research Consortium Member Sam Gandy Develops New Research Approach -- Yields Exciting Results on Origins of Alzheimer's

Research consortium member, Dr. Sam Gandy, has developed a new approach for studying brain synapses that has begun to yield valuable information about the production of Amyloid-Beta oligomers, known to play a role in the onset of Alzheimer's disease.

By better understanding how Abeta clumping is regulated, researchers can learn how to prevent, stop or slow Alzheimer's pathology.

Dr. Gandy's research, founded by Cure Alzheimer's Fund, was published in the March 17th issue of the Journal of Neuroscience. Click here to read the article in its entirety.


New Approach Yields Exciting Results on Origins of Alzheimer’s Disease: Testing of New Drug to Block Alzheimer's Causing Abeta42 Aggregation Underway

Boston -- A new approach developed for studying brain synapses has yielded valuable information about the production of Amyloid-Beta oligomers (clumps of the Abeta peptide) known to play a key role in the onset of Alzheimer’s disease.

Published in the March 17 issue of the Journal of Neuroscience and funded by Cure Alzheimer’s Fund (CAF), the research of Dr. Sam Gandy, Professor in Alzheimer’s disease Research at the Mount Sinai School of Medicine and a member of the CAF research consortium, and his colleagues, could uncover a new lead in the fight for prevention of this devastating disease.

“It is crucial that we understand how Abeta clumping is regulated, especially at the synapse, if we are to learn how to prevent, stop or slow Alzheimer’s pathology. Abeta42 is believed to be the first subtype of the Abeta peptide to oligomerize (clump together), and therefore most harmful to the brain,” Gandy said. “Now that the neurotransmitter receptor, ‘Group II mGluR’, has been identified as a source of Abeta42, we can find ways to reduce Abeta42 generation at the synapse. Lowering levels of Abeta42 would be predicted to hinder formation of poisonous clumps (oligomers).”

Gandy’s new approach is based on the use of isolated intact nerve terminals (synapses) from mice bred specially using human AD genes. Soong Ho Kim, a postdoctoral fellow in Gandy’s lab, has pioneered this approach. The new system aided in isolating a particular receptor at the synapse, known as “Group II Metabotropic Glutamate Receptor” (or mGluR). Group II mGluR selectively controls the formation Abeta42 at the synapse.

Studies have shown Abeta and its variant Abeta42 play a critical role in Alzheimer’s pathology. Previous research backed by CAF has shown that Abeta42 oligomers are formed at the neuronal synapse, a specialized way station where messages pass from one nerve cell to the next cell in the circuit. Disruption of synapses by Abeta42 oligomers is believed to underlie the loss of brain function in AD.

In unrelated work, a neuroscience bio-tech company, in the process of researching anti- depressants, has developed a safe and orally active drug that blocks ‘Group II mGluR’. In light of Gandy’s new discoveries, he and his colleagues are using the new synaptic terminal system to test the drug before moving on to test mice to determine if the drug can block Abeta from aggregating, which could be a leap forward in the search for preventative therapies.

“The development of this innovative approach by Dr. Gandy and his team could open up new doors of research on this devastating disease,” said Tim Armour, President and CEO of Cure Alzheimer’s Fund. “It’s an important step in understanding and ultimately slowing, stopping or even reversing the effects of Alzheimer’s disease.”

Less Than 1 Month Until the Big Day!

A message from race organizer Barbara Geiger:

Who said planning a race would be easy? We knew it wouldn't be. Between kids, husbands, games, work, dinner, homework, one cat and one dog; life was already chaotic enough.

But we also know it will all be worth it.

All the elements are falling into place for April 10th. We have secured a most generous Presenting Sponsor, Tri-Coastal Design of East Hanover, NJ.  Our other sponsors have donated water, fruit, brochures and posters.  We even have a distinguished guest speaker for our morning program, New Jersey State Senator Richard Codey!

What needs to happen next?

Tying up some loose ends, gathering our volunteers for the day and most importantly, signing up more walkers and runners. We have good momentum and some great marketing strategies in place to get the word out. Now we need participants. We are confident they will come, but we’re asking everyone to get the word out.

If you are in Northern New Jersey on Saturday, April 10th, come join us in Roseland, NJ for the 1st Annual Running 4 Answers!

Dr. Rudy Tanzi's Breakthrough Research Featured in New York Times

Breakthrough research conducted by our very own Dr. Rudy Tanzi and his team at Massachusetts General Hospital has led to an important advancement in the understanding of the protein associated with Alzheimer’s disease.

The prevailing theory has been that this protein -- A-beta -- has no function other than as a waste product created by the brain. But Dr. Rudy Tanzi's team at Harvard suggests that the protein is part of the brain's innate immune system -- defending against bacteria and other microbes.

The innate immune system is also triggered by traumatic brain injuries and strokes -- occurrences known to increase one's risk of Alzheimer's. So what exactly is the relationship between the brain's response to infection and Alzheimer's disease? Dr. Tanzi and his team have more work to do, but the findings have researchers impressed.

"It changes our thinking about Alzheimer's disease," Dr. Eliezer Masiah, who heads the experimental neuropathology laboratory at University of California, San Diego. "I don't think we ever thought about that possibility for A-beta. I think he's onto something important."

To read the complete article, visit