News

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

Slides from the Webinar

Thank you to those who attended our Webinar on July 22 titled “Working Toward a Cure for Alzheimer’s: Clues from our Genes”. Below are the slides from the event. Video clips addressing key components of the presentation and blog posts responding to questions from the webinar will be posted shortly.

Click each slide to advance.

Brain Scan Diagnostics for early detection of Alzheimer’s --- a good idea?

There is debate about this.  A panel of leading Alzheimer’s researchers has recommended new guidelines for earlier diagnosis of Alzheimer’s Disease (AD), including the use of brain imaging.  While most commentators have hailed this news, a few have raised concerns. One of the clearer expositions of this was a Forbes online blog by Robert Langreth on July 15 entitled “A Scary Idea: Pre-emptive Brain Scans for Alzheimer’s.”

Langreth hypothesizes this diagnostic report:
“You feel fine and have no symptoms, but your brain is slowly rotting away. And there is nothing we can do about it.” Maybe he should have added “now”.

What is behind all this, and is this proposal really useful for patients and research?

"CAF's Sam Gandy delivers "Hot Topics" session at International Conference on Alzheimer's Disease (ICAD)"

At ICAD 2010 in Hawaii Dr. Sam Gandy of Cure Alzheimer's Research Consortium presented the results of a study showing a new class of biomarkers that can stick to protein structures in the body and emit colors reflecting the different shapes or forms of the proteins. They are called luminescent conjugated oligothiophenes (LCOs) or luminescent conjugated polymers (LCPs). Among other uses, they are currently being employed in test tubes, animal models and autopsied Alzheimer’s brains to study the structure of protein deposits caused by the disease. The new markers bind to the two well-established hallmarks of Alzheimer’s – beta amyloid plaques and tau tangles – and glow different colors depending on which forms of the deposits they “stick” to (e.g., plaques often “glow” orange, while tangles glow yellowish green).

Webinar on July 22: "Working Toward a Cure for Alzheimer's: Clues from our Genes" with Doctor Rudy Tanzi

Join us for our 2nd annual webinar on June 22. We will be hosting Dr. Rudy Tanzi, who will present his latest findings in the field of Alzheimer’s disease genetic research. The presentation will include a brief history of Alzheimer’s disease research, an explanation of the Alzheimer’s Genome Project, as well as the introduction of his new research on abeta as an anti-microbial agent.

Click HERE to register.

If you are unable to attend the webinar, e-mail us at info@curealz.org and we will send you a podcast of the event.

Dr. Rudy Tanzi is the Joseph P. and Rose F. Kennedy Professor of Neurology at the Harvard Medical School and the Director of the Genetics and Aging Research Unit at Massachusetts General Hospital. He has been investigating neurodegenerative disease since 1980 when he participated in the pioneering study that led to the location of the Huntington disease gene. He has identified several Alzheimer’s disease genes, including the first Alzheimer’s gene, the beta-amyloid protein precursor (APP). His work in the Alzheimer’s Genome Project, which has identified other new Alzheimer’s genes, was recognized by TIME magazine as one of the top 10 medical breakthroughs of 2008. Dr. Tanzi is a world-renowned leader in the studies of Alzheimer’s disease genetics.

The event will be held online, with each participant connecting through their own computer and telephone. More information on the webinar process can be found at www.gotowebinar.com

If you have any further questions, please contact us Katie Cutler at kcutler@curealz.org

McCance presents at Venture Summit East 2010

Henry McCance, Cure Alzheimer’s Fund co-founder and chairman emeritus, Greylock Partners, was a keynote speaker at Venture Summit East 2010. This two-day gathering highlighted the significant economic, political and technology trends impacting the global growth investor and was held at Harvard Business School. Venture Summit East features the most influential institutional investors, venture capitalists, corporate buyers, investment bankers and research analysts in the eastern United States in keynote presentations and panel debates.

Henry’s presentation featured ideas about how to use a venture capital approach to solve world problems. He focused on Alzheimer’s, citing the scope of the problem and Cure Alzheimer’s Fund’s innovative and targeted approach to end the disease.

Peek and Treat: A Pioneering Collaborative Research Project

Despite advances in understanding the pathology of Alzheimer’s disease, advancements in its diagnosis and treatment are limited. To address this key need, researchers at the University of Texas Health Science Center at Houston (UTHealth) and the University of Houston(UH) have been awarded a $150,000 grant from Cure Alzheimer’s Fund to pursue innovative work.

Tjan highlights venture capital approach to research

Tony Tjan, a member of our advisory board, recently wrote a blog post on the innovative field of medical research entrepreneurship. He highlights our effort to take a venture capital approach in order to improve what is currently a broken research system.

The medical research model as we know it today is broken. Why? Three words: insufficient, inefficient, and ineffective. This is both the big problem and the big opportunity for medical entrepreneurship. Today's model is insufficient because typically 1% or less of the amount spent each year on diseases goes towards cure research, with the balance going to caring for people with the disease. Alzheimer's, for example, costs our country hundreds of millions of dollars each year, yet we spend just one cent out of every $4.00 available towards a cure.

You can read the rest of this article, and other posts on the topic of entrepreneurship, at his Harvard Business Review Blog.

Economist agrees we need to invest in research!

The prestigious Economist weighs in on the “pooling of drug test data” discussion (Wall Street Journal, “Drug Makers Will Share Data From Failed Alzheimer’s Trials”, June 11, 2010) and agrees with Cure Alzheimer’s Fund: the emphasis should be on research that finds the cause of the disease rather than spending billions on the development of drugs that may be addressing the wrong targets or the right targets in the wrong ways. To quote the Economist, “the problem of what causes Alzheimer’s is profound” and so far, unresolved. In fact, as the article points out, fundamental perspectives on the causes of the disease are changing right now, and to at least some extent obviating the billions spent on drugs developed from very imperfect information about the basic pathology of Alzheimer’s.

It is a very hard problem to solve, but, again as the Economist states, “it is the “R” rather than the “D” of research and development that needs to be emphasized at the moment.” We at CAF couldn’t agree more with the Economist’s conclusion that now is the worst time to be cutting back on the “R”, which, in fact, NIH is doing.  The numbers that are increasingly well known are staggering and depressing. The United States will spend roughly $170 billion on care for Alzheimer’s patients in 2010, but invest only about $480 million in research into the causes of the disease through the National Institutes of Health in 2011. Shockingly that number is DOWN from $643 million in 2006.

As the Economist summarizes, “you get what you pay for”. Unless we rebalance this equation of care spending to cure spending, the future for the roughly half of people over 85 who have the disease or will get it in the next ten years is bleak indeed.

Real progress IS being made

In Response to Nicholas Wade’s NYT column, June 12, 2010:
“A Decade Later, Genetic Map Yields Few New Clues”
But real progress IS being made.

 

The promised breakthroughs and cures from the Human Genome Project may have been too optimistic from a timing perspective. But Wade may be too pessimistic when he writes, “Indeed, after ten years of effort, geneticists are almost back to square one in knowing where to look.”

Not really. As others in the piece say, the Human Genome Project and the HapMap project growing out of it have been essential to a better understanding of the genetic underpinning of many common diseases.  The evidence is clearly with Eric Lander who says in the article, “Having a common scaffold on which one can put all the information has dramatically accelerated progress.”

But why no cures yet? Because in plotting the genetic map, we learn that each step taken teaches us more as well as opens more questions to be resolved. For example, researchers have found that what was commonly regarded as “junk” between pieces of DNA isn’t “junk” at all; it has functions that contribute to biological processes just as the DNA does. And one of the bigger surprises has been that knowing the common genetic variants isn’t enough to find the causes of disease. Researchers must track down the rare variants or mutations with strong biological effects on the disease.  As Wade writes, “It now seems more likely that each common disease is mostly caused by large numbers of rare variants, ones too rare to have been cataloged by the HapMap.”

Yes; this is a very important finding, and one that would have been years ahead of us without the Human Genome Project and HapMap.  And this positions us well to take the next steps to reduce the time for development of effective therapies. Rudolph Tanzi, PhD, head of the Genetics and Aging Unit at Mass General Hospital and primary investigator of the Alzheimer’s Genome Project funded exclusively by Cure Alzheimer’s Fund, says: “Having identified over 200 new Alzheimer’s candidate genes through the Alzheimer’s Genome Project, we can now find the ‘causal’ DNA variants in Alzheimer’s, then determine which biochemical pathways are broken as a result, and discover therapies to “fix what is broken” based on that information.”

Another recent article in the Wall Street Journal reports that “Drug Makers Will Share Data for Failed Alzheimer’s Trials” (WSJ, June 11, 2010). Why so many failures? One major reason is that many of these drugs were developed without the knowledge of these genetic processes and their biological effects.

Yes, it takes time --- and much more money than has so far been dedicated to Alzheimer’s research --- to discover what genetics has to teach us about the basic causes of disease. But without following that trail, the cost and the failure rate will be much, much higher.

Sharing Data is Good But We Need to Better Understand Causes of the Disease

The Wall Street Journal, Reuters, and other publications carried an important story on June 11 indicating that “drug makers will share data from failed Alzheimer’s trials” to try to determine “what is wrong with the studies and what can be done to improve drug development.” (WSJ, Drug Makers Will Share Data From Failed Alzheimer’s Trials, June 11, 2010).

The short answer was given in that article by Ray Woosley, MD, chief executive of the Critical Path Institute: “We really believe drugs are failing because we honestly do not understand the disease.” YES! That is the truth. How can you make effective therapies when you don’t understand what causes the disease in the first place?

While pooling data and sharing resources is certainly a useful idea, an even more effective strategy would be to spend more time and money to understand the causes of the disease. Cure Alzheimer’s Fund is committed to the simple proposition that understanding the disease’s cause is the fastest path to a cure. And for Alzheimer’s, the story clearly begins with the genes. When Cure Alzheimer’s Fund was incorporated in late 2004 only four genes had been conclusively shown to modulate Alzheimer's progression. In addition, the association of three of the four genes was restricted to early onset Alzheimer’s, which accounts for fewer than 5 percent of Alzheimer’s disease patients. The fourth gene was associated with the much more prevalent late onset form of Alzheimer’s. However, this fourth gene accounted for less than 30 percent of the genetic component of late onset Alzheimer's. For more than 95 percent of Alzheimer's cases, the bulk of the contributing genetic factors remained unknown.

In 2005, Cure Alzheimer’s Fund committed to finding the remaining Alzheimer’s –associated genes, and to investigating promising novel therapies based on information learned from the first four genes. To this end, Cure Alzheimer’s Fund established and committed $4 million over 4 years to a new initiative named the Alzheimer’s Genome Project. Aided by the advent of the human genome map, the availability of new technology for gene identification and sequencing, and our researchers’ pioneering use of advanced statistical analysis we achieved what we believe is a great leap forward in the hunt for Alzheimer's causing genes. The Alzheimer’s Genome Project has identified over 200 new candidate genes in the first four-year phase.

Having the right set of targets as identified by careful and comprehensive genetic studies dramatically decreases the development time to a cure. For example, building from genetic research, investigators supported by Cure Alzheimer’s Fund have identified how aggregates of the “bad guy” Alzheimer’s protein, Abeta42, aggregate to create a hyper-toxic environment for neural synapses in the brain and how compounds originally designed to lower cholesterol may be effective in lowering Abeta42 in the brain. Most remarkably, recent research by Cure Alzheimer’s Fund supported scientists has demonstrated that the same Abeta42 that has been seen as the arch-villain in the Alzheimer’s play may in fact be part of the innate immune system of the brain, and therefore a “hero” gone bad under certain circumstances! This is paradigm-changing research.

All of which is to say that spending billions on drug development when the target of the drugs is still poorly understood is bound to result in, at a minimum, disappointment. See our article on “Why the Drugs Don’t Work” in the Cure Alzheimer’s Fund Quarterly Report for Q1, 2010 for specific information about why certain drugs have failed and what research is proving more fruitful.

In the meantime, pooling data from failed trials is certainly useful, but an even more efficient and effective strategy would be to put more attention, effort and money into understanding the basic causes of the disease.