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Over the past three years, progress in the molecular genetics of familial Alzheimer's disease has been fast and fundamental. The seminal finding that some cases are due to a mutation in the β-amyloid precursor protein (APP) gene has been followed by the discovery of a major additional locus for the disease on chromosome 14. The combined data suggest that the genetic sites accounting for most early-onset familial Alzheimer's disease cases have now been located. In addition, research is revealing the mechanisms by which the genes exert their pathogenicity. This promises to provide the explanatory link between the genes and the clinicopathological syndrome. The ultimate goal, an understanding in similar terms of the much commoner senile, sporadic form of Alzheimer's disease, is now a realistic target.

Original publication




Journal article


British Journal of Psychiatry


Royal College of Psychiatrists

Publication Date





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