Abstract
In early 1993, the genetic data implicating the amyloid precursor protein as one of the loci leading to early onset Alzheimer's disease were reviewed (Hardy and Duff, Annals of Medicine, 25: 437-440), together with the evidence implicating abnormal deposition of beta-amyloid as the initiating point of the process leading to the disease. Since that time, three other genetic loci have been directly implicated in the aetiology of the disease: the apolipoprotein E locus on chromosome 19, the presenilin 1 gene on chromosome 14 and the presenilin 2 gene on chromosome 1. In this article, I review the progress over the last three years and attempt to assess whether the evidence for the amyloid cascade hypothesis still stands scrutiny.
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