Familial Alzheimer's disease:: Oxidative stress, β-amyloid, presenilins, and cell death

被引:13
|
作者
Velez-Pardo, C
Del Rio, MJ
Lopera, F
机构
[1] Univ Hosp, Dept Neurol, Medellin, Colombia
[2] Univ Antioquia, Sch Med, Medellin, Colombia
来源
关键词
familial Alzheimer's disease; presenilin-1; oxidative stress; E280A mutation; RAGE; beta-amyloid;
D O I
10.1016/S0306-3623(98)00189-X
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
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 sustitution 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. (C) 1998 Elsevier Science Inc.
引用
收藏
页码:675 / 681
页数:7
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