Cure Alzheimer's Fund: Targeting Breakthrough Research

Groundbreaking Study: Alzheimer’s-associated gene may be part of innate immune system

Tuesday, 02 March 2010 20:24

From Cure Alzheimer's Fund President & CEO, Tim Armour:

Exciting news!

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.

According to Dr. Tanzi’s research, which will be featured in tomorrow’s issue of PLoS One, amyloid-beta protein (A-beta) -- the primary constituent of the plaques found in the brains of Alzheimer’s patients -- may be a normal part of the innate immune system.

“These data change the way we look at A-beta. For years we thought that A-beta was just metabolic garbage produced as a byproduct of other processes within the brain, but these data suggest it is a normal component of the brain’s innate immune system,” says Dr. Tanzi. “If we can manage the production of A-beta in the brain’s innate immune system triggered by combinations of genetics and environmental factors, we may be able to lower the risk for this devastating disease.”

This is a significant breakthrough in the search for a cure! By better understanding A-beta, our researchers can more effectively develop preventative and therapeutic strategies -- bringing us that much closer to eliminating Alzheimer’s once and for all.

And with 78 million Baby Boomers quickly approaching the age of greatest risk for Alzheimer's, we must find a cure fast!

For the last 5 years, we’ve invested in research that is speed-driven, results-oriented and innovative. It’s this unique approach that has paid off handsomely in the past and again today -- thanks largely to your continued support.

Every dollar of new funds leads us closer to understanding and eliminating this disease. If you haven’t made a gift to the Cure Alzheimer’s Fund, please consider making a gift today to help end Alzheimer’s in our lifetimes.

Following the A-beta Trail

Tuesday, 02 March 2010 13:48

Most researchers agree that the amyloid beta peptide, A-beta, is a key player in Alzheimer’s disease pathology. Exactly how it is involved is still unclear; but attention is now shifting from A-beta as the main component of the tell-tale amyloid plaques to the basic component in A-beta “oligomers” or clumps of the A-beta peptide which have been shown to be toxic to cells in the brain that receive and process messages involving memory.

The editorial by Sam in the March 1 online issue of The Lancet Neurology, accompanies a research article written by lead author Juha O Rinne and colleagues that uses neuro-imaging to see the results of the application of a drug now in trials called bapineuzumab (short for beta-amyloid peptide neutralizing monoclonal anti-body) by Elan/Wyeth. The straightforward discovery is that neuro-imaging can detect in vivo that a study drug is able to lower the presence of A-beta, and therefore possibly be effective against Alzheimer’s disease pathology.

The authors demonstrate that, in fact, neuro-imaging does show that the drug bapineuzumab “reduces the cortical fibrillar amyloid-beta load in Alzheimer’s disease” by about 25% over a 78 week period.

However, Sam highlights the fact that this study, as well as others, report “little or no obvious clinical response to bapineuzimab.” In other words, the drug may have caused the amount of the A-beta peptide to go down, but that did not result in any clinical difference or improvement in the patients tested over 78 days.

According to the “amyloid hypothesis” as it is understood by many, an observed reduction in the A-beta load should result in a decrease in Alzheimer’s pathology, presumably evidenced by improvement in cognition, stabilization of the rate of cognitive decline, or relief of other symptoms in treated patients. What’s going on here?

At its most extreme, one conclusion could be that the “amyloid hypothesis” is bunk. We’ve had several drugs in trials that target reduction in A-beta, but none seem to improve cognition or other symptoms to any appreciable degree. So A-beta must be the wrong target.

But wait, says Sam, there are other things going on here. First, Sam notes that neither of the so-called “failed” anti-amyloid trials actually measured amyloid buildup, which, he goes on to say, “would be like testing a statin…without measuring (its effect on) cholesterol”. He also reminds us that genetic analysis keeps leading us back to A-beta, concluding that there “are compelling, unchangeable facts suggesting involvement of amyloid beta in genetic forms of Alzheimer’s disease.” Furthermore, Sam says, “logic dictates that amyloid beta cannot be causative and toxic in genetic forms of the disease and yet totally harmless and irrelevant in common sporadic forms.” Long term prevention studies will be required to settle this conundrum, argues Dr. Gandy.

Furthermore, if we go back to the emerging theory of the importance of A-beta “oligomers” in Alzheimer’s pathology, we have another puzzle. The imaging technology so far cannot “see” oligomeric A-beta. Therefore, it could be that both the drug and the imaging are aiming at the wrong kind of A-beta targets!

Sam therefore suggests that even though tests of the kind described in this paper may raise questions about the “amyloid hypothesis,” and may not be able to demonstrate the effectiveness of some drugs currently being tested, there are other drugs in the pipeline that do have, at least initially, a positive effect on Alzheimer’s symptoms and may be addressing a different “mechanism of action” that most drugs up until now have targeted. These new drugs include the Russian drug developed as an anti-histamine, Dimebon (recently re-named “latrepirdine”), now in Phase 3 trials, which appears to accelerate clearance of A-beta before oligomers are able to form. Sam points out recent work from his own lab (supported by CAF) suggesting such a model as well as recent work by Sergey Bachurin (the “father of Dimebon”) in a Russian journal showing that Dimebon clears out deposits of the protein that causes Parkinson’s disease. Could it be, Sam asks, that Dimebon stimulates cells to break down oligomers?

Clearly much more work needs to be done; but to place all our chips on one theory of how A-beta affects Alzheimer’s pathology, or to throw the theory out completely because it does not lead to effective results based on our previous read of how A-beta affects Alzheimer’s pathology would be, as Sam says, “irrational and irresponsible.”

More and more, it is becoming clear that following the A-beta trail, rooted in strong genetic evidence, provides the right roadmap to a cure.

To read Sam's editorial, click here.

Save health care -- Invest in research

Monday, 22 February 2010 13:49

From Cure Alzheimer's Fund President & CEO, Tim Armour:

Last week, I told you all that our federal government will spend $2 trillion on Alzheimer’s care in this decade alone. What I didn’t tell you was that while we will spend $184 billion on care in 2010, we will only invest $430 million on research -- not even 1% of what we’re spending on care!

This is a recipe for disaster – not only for the well-being of future generations, but for our entire health care system. How much longer can we delay progress toward a cure before we bankrupt the entire health care system?

We must rebalance this equation. Please join me in telling Congress to make a national commitment to a cure – and ask your loved ones to do the same.

http://salsa.wiredforchange.com/o/5850/t/5223/petition.jsp?petition_KEY=755

We are a nation that takes care of its own and we must continue to care for those in need now – funding for Alzheimer’s care is critical. But we can’t continue to ignore the facts.

We are pouring billions of dollars into just treating the symptoms of the disease when we know we can cure it. It doesn’t make any sense. We have the roadmap to a cure – that's what makes us unique – now we just need the funds to make it happen.

The American people deserve health care that is effective and sustainable. Join us and together we’ll find a cure to this debilitating and economically crippling disease.

And as always, thanks for everything you do to help us find a cure!

Climbing for a Cure

Written by Katie Barr Friday, 19 February 2010 11:51

We first introduced you to Alan Arnette back in 2007 when he embarked upon an adventure he called “The Road Back to Mount Everest: Memories are Everything.” He spent the yearlong journey climbing 5 of the world’s highest mountains to raise money for Cure Alzheimer’s Fund -- and we couldn’t be more thankful!

But Alan isn’t done yet and this time his sights are set on an even bigger goal -- climbing the world’s biggest mountains to raise $1 million for Alzheimer’s research!

“The Seven Summits” is no small feat, but Alan is ready for the challenge. An experienced climber, Alan says this mission isn’t just about climbing, it’s about trying to find a cure for the disease that took the lives of his mother and 2 aunts -- and 100% of every dollar Alan raises will go directly to the research that will eventually cure this devastating disease!

So what exactly lies ahead for Alan? He will climb Mount Kilimanjaro (19,563 feet) this summer and then on to:

• Denali, 20,320 feet, in Alaska
• Elbrus, 18,481 feet, in Russia
• Everest, 29,035 feet, in Nepal
• Aconcagua, 22,841 feet, in Argentina
• Vinson, 16,850 feet, in Antarctica
• Mount Kosciuszko, 7,310 feet, and Carstensz Pyramid, 16,023 feet, on Irian Jaya, in Australia/Oceania

If you want to learn more about Alan and his quest to raise $1 million for Alzheimer’s research, visit him at www.alanarnette.com or check out the Loveland Reporter Herald’s recent piece on Alan!