There has been a spate of announcements about promising drug therapies, “new” genes and environmental factors affecting Alzheimer’s disease (AD) in the news lately. These are likely to increase as the media becomes more sensitized to the looming disaster that Alzheimer’s presents to the world.
We thought it would be useful to bring you up to date on our research agenda. Cure Alzheimer's Fund’s supported research is active in basic genetic research and early stages of drug development, and also addresses several key environmental factors.
Our core effort is the Alzheimer’s Genome Project™ initiative. Using “whole genome association” on over 1400 AD families, the latest gene-testing technology and most advanced statistical techniques, our objective is to identify all the genes that affect risk for AD. Instead of hunting for novel AD genes one at a time, we are endeavoring to identify as many as possible simultaneously to provide an understanding of which genes among all are the most important in conferring either risk for or protection against AD. Genes identified by other labs will also be tested in our whole genome scan—no viable candidate from any source will be excluded—and we’ll look at the resulting set of AD genes as a whole, not piecemeal. The biological pathways elucidated by these genes should then provide clear targets for effective research into the pathological underpinnings of the disease and for novel therapies aimed at treating or preventing AD.
2. Drug Development
While not developing drugs per se, from the basics of genetics, Cure Alzheimer’s Fund supports researchers who are exploring promising mechanisms for effective pharmacological intervention as well as looking at the effect that existing, repositioned drugs may have on the disease. An example of the former is the research into “Abeta oligomers” being done collaboratively by several members of our Research Consortium and other invited researchers. This truly “breakthrough research” is making great progress in understanding how clusters of the Abeta 42 molecule interfere with key neuronal synapses in the brain—which more researchers are coming to think signals the real beginnings of the disease. Cure Alzheimer’s Fund is supporting a second and expanded year of this research; for details see the Research section on our website.
A second example in this category is Cure Alzheimer’s Fund’s support for research on an ACAT inhibitor, a drug originally developed for anti-cholesterol use, but which may prove effective in lowering Abeta 42 counts in the brain as well.
A third example of work in the area of drug development is with vaccines. See Dr. David Holtzman’s overview of the AD vaccine story in our Quarterly Report Fall 2006.
Two key findings by Cure Alzheimer’s Fund researchers speak to the AD environmental issues in the news. One is the value of physical exercise. One of the earliest papers on this topic was done by Sam Sisodia, Ph.D., who provided us with an overview in our Quarterly Report Spring 2007.
The second environmental issue is the impact of stroke and traumatic brain injury (TBI) on AD. Researchers long have thought there is an association between the effect of stroke or TBI and AD, but have been unable to identify the linking mechanism. A recent paper by a group of researchers at Massachusetts General Hospital, including Rudy Tanzi, Ph.D., shows a clear link between a particular enzyme and the debilitating effects of stroke and TBI. That particular enzyme is also a key actor in the AD story. For more details, please visit our website, click on the “Press Room” link at the top and look under “Latest News Coverage ” for a review of this paper in Medical News Today (6/10/07).
Alzheimer’s is in the news, and Cure Alzheimer's Fund continues to be part of it. We will continue to work on the big stories, true “breakthrough research” that will make a difference in all our lives. Stay tuned.