Research Team Identifies Gene That Appears To Increase Alzheimer’s Risk

Adapted from The Translational Genomics Research Institute

A study comparing genetic markers in the DNA of people with and without Alzheimer’s disease has enabled researchers to identify a common gene that appears to increase a person’s risk for developing Alzheimer’s disease. The finding, announced today by researchers at the Translational Genomics Research Institute (TGen), Banner Alzheimer’s Institute, Kronos Science Laboratory and their collaborative partners, suggests that the gene—called GAB2—modifies an individual’s risk when associated with other genes, including APOE4. The study results appear in the June 7, 2007 issue of the prestigious peer-reviewed journal, Neuron.

“We have entered a new era in medical research. Today’s 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 TGen’s Neurogenomics Division and the paper’s senior author, “These new, robust tools may eventually allow us to improve our ability to diagnose Alzheimer’s disease, even before it strikes.”

To date, the most significant gene found to predispose an individual to late-onset Alzheimer’s has been APOE4. In this latest study, researchers from seven organizations contributed to the genome-wide scan. The team screened the DNA from 1,400 individuals who had been clinically assessed with Alzheimer’s prior death, and simultaneously examined more than 500,000 genetic variations to characterize and confirm additional late-onset Alzheimer’s disease susceptibility genes. The search revealed GAB2.

Based on the genetics of this and other scientific findings, researchers suggest the healthy form of the GAB2 gene may protect brain cells from developing tangles, one of the hallmarks of Alzheimer’s disease. If the findings are confirmed, this discovery could provide a target for future Alzheimer’s therapeutic drugs.

“We hope that this study, along with the genome-wide genetics studies to come, will contribute to the clarification of Alzheimer’s risk factors and disease mechanisms, the discovery of promising new disease-slowing and prevention therapies, and the identification of patients and at-risk people most likely to benefit from those treatments,” said Dr. Eric Reiman, the study’s first author and Executive Director of the Banner Alzheimer’s Institute.

 

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