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Breakthrough Mapping of Alzheimer's Genome Helps ID Four New Suspect Genes
Date:10/30/2008

BOSTON, Oct. 30 /PRNewswire-USNewswire/ -- Four novel genes that may significantly increase the risk of the most common form of late-onset Alzheimer's have been identified by researchers at Massachusetts General Hospital and Harvard Medical School, as reported in the November 7th issue of American Journal of Human Genetics. The findings, part of a larger "Alzheimer's Genome Project" (AGP) established three years ago to identify the full set of Alzheimer's disease genetic risk factors, may lead to more aggressive therapeutic interventions to slow, stop or even reverse the effects of the disease. These new therapies would differ from current treatments that only address the symptoms of the disease.

Dr. Rudolph Tanzi, chairman of the Cure Alzheimer's Fund Research Consortium and the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard Medical School, completed the largest family-based genome-wide association screen conducted to date. More than 400 families affected by Alzheimer's disease were screened to determine genetic variants associated with the inheritance of Alzheimer's. The four genes discovered in the family study are described in the article.

Technological advances are improving the understanding of the genetic mechanism that governs Alzheimer's disease and are making it feasible to identify the complete set of genes influencing risk for Alzheimer's disease, Dr. Tanzi said.

In addition to the genome-wide association screen, Dr. Tanzi and Dr. Lars Bertram of Harvard Medical School have been analyzing Alzheimer's genetics literature to determine which of the hundreds of proposed Alzheimer's candidate genes are genuine disease genetic risk factors. These summarized findings, implicating 30 gene candidates, are updated regularly at http://AlzGene.org (a public Web site sponsored by the Cure Alzheimer's Fund). Tanzi and Bertram highlighted 10 of the most interesting of these gene
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SOURCE Cure Alzheimer's Fund
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