PHOENIX, June 6, 2007 -- A study comparing more genetic markers in the DNA of people with and without Alzheimers disease than ever before has enabled researchers to identify a common gene that appears to increase a persons risk for developing Alzheimers disease. The finding, announced today by researchers at the Translational Genomics Research Institute (TGen), Banner Alzheimers Institute, Kronos Science Laboratory and their collaborative partners, suggests that the gene called GAB2 modifies an individuals risk when associated with other genes, including APOE4. The study results appear in the June 7 issue of the prestigious peer-reviewed journal, Neuron.
Alzheimers disease is the most common form of disabling memory and thinking problems in older people. The progressive neurological disorder afflicts an estimated 5 million Americans, a number expected to triple by 2050.
We have entered a new era in medical research. Todays technologies permit us to survey a sufficient number of letters throughout the human genome to provide a clearer picture of how life works and ultimately allow better clinical management of patients, said Dr. Dietrich Stephan, Director of TGens Neurogenomics Division and the papers senior author, These new, robust tools may eventually allow us to improve our ability to diagnose Alzheimers disease, even before it strikes
To date, the most significant gene found to predispose an individual to late onset Alzheimers (LOAD) has been APOE4. In this latest study, researchers from seven organizations contributed to the genome-wide scan using Affymetrix microarray technology. The team screened the DNA from 1,400 individuals who had been clinically assessed with Alzheimers prior death, and simultaneously examined more than 500,000 SNPs or genetic variations to characterize and confirm additional LOAD susceptibility genes. The search revealed GAB2.
Based on the genetics of this and other neuroscientific findings,
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Contact: Galen Perry
gperry@tgen.org
602-343-8423
The Translational Genomics Research Institute
6-Jun-2007