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Review
. 1998 Nov;31(5):675-81.
doi: 10.1016/s0306-3623(98)00189-x.

Familial Alzheimer's disease: oxidative stress, beta-amyloid, presenilins, and cell death

C Velez-Pardo  1 , M Jimenez Del Rio, F Lopera
Affiliations
Review

Familial Alzheimer's disease: oxidative stress, beta-amyloid, presenilins, and cell death

C Velez-Pardo et al. Gen Pharmacol. 1998 Nov.

Abstract

1. The basic etiology of Alzheimer's disease remains unknown, although four genes have so far been involved: beta-amyloid precursor protein, presenilin-1, presenilin-2 and apolipoprotein E genes. 2. The largest familial Alzheimer's disease (FAD) kindred so far reported belong to a point mutation in codon 280 that results in a glutamic acid-to-alanine substitution in presenilin-1 characterized in Antioquia, Colombia. 3. A hypothetical unified molecular mechanism model of cell death in FAD mediated by presenilin-1, beta-amyloid, and oxidative stress is proposed as an attempt to explain the mechanisms of neuronal loss in this neurodegenerative disorder.

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