Alzheimer’s disease is an irreversible, progressive brain disorder that occurs gradually and results in memory loss, behavior and personality changes, and a decline in cognitive abilities. Studies during the last several years have demonstrated there is a genetic component, but until 2001, only four genes were conclusively known to be associated with the disease. Three genes—amyloid precursor protein, presenilin 1, and presenilin 2—are linked to the early onset form; are autosomal dominant; and account for only a small number of all Alzheimer's disease cases. Studies on the more common late-onset form of Alzheimer's disease have shown that a fourth gene, the APOE gene, is a susceptibility factor for sporadic late-onset Alzheimer's disease. Recent reports have suggested there are additional risk factor genes for late-onset Alzheimer's disease, and new Alzheimer's disease-related regions in the human genome and gene candidates have been identified that may modify the risk for Alzheimer's disease. This advisory meeting highlighted the newest findings in the genetics of late-onset Alzheimer's disease.
Speakers at this meeting included: Drs. Alison Goate; Margaret Pericak-Vance (Duke University); Peter St. George-Hyslop (University of Toronto); Gerard Schellenberg (University of Washington); Lindsay Farrer (Boston University School of Medicine); Rudy Tanzi (Harvard and Massachusetts General Hospital); Stephen Younkin (Mayo Clinic, Jacksonville); and Steve Estus (University of Kentucky).
Drs. Marilyn Miller and Stephen Snyder