Is oxidative damage the fundamental pathogenic mechanism of Alzheimer's and other neurodegenerative diseases?

被引:257
作者
Perry, G
Nunomura, A
Hirai, K
Zhu, XW
Pérez, M
Avila, J
Castellani, RJ
Atwood, CS
Aliev, G
Sayre, LM
Takeda, A
Smith, MA
机构
[1] Case Western Reserve Univ, Inst Pathol, Cleveland, OH 44106 USA
[2] Asahikawa Med Coll, Dept Psychiat & Neurol, Asahikawa, Hokkaido 078, Japan
[3] Takeda Chem Ind Ltd, Pharmaceut Res Labs 1, Osaka 532, Japan
[4] Univ Autonoma Madrid, Ctr Biol Mol, E-28049 Madrid, Spain
[5] Case Western Reserve Univ, Dept Chem, Cleveland, OH 44106 USA
[6] Case Western Reserve Univ, Dept Anat, Cleveland, OH 44106 USA
[7] Tohoku Univ, Sch Med, Dept Neurol, Sendai, Miyagi 980, Japan
关键词
Alzheimer's disease; amyloid-beta; antioxidants; homeostasis; neurofibrillary tangles; oxidative stress; redox balance; senile plaque; tau; free radicals;
D O I
10.1016/S0891-5849(02)01113-9
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In less than a decade, beginning with the demonstration by Floyd, Stadtman, Markesbery et al. [1] of increased reactive carbonyls in the brains of patients with Alzheimer's disease (AD), oxidative damage has been established as a feature of the disease. Here, we review the types of oxidative damage seen in AD, sites involved, possible origin, relationship to lesions, and compensatory changes, and we also consider other neurodegenerative diseases where oxidative stress has been implicated. Although much data remain to be collected, the broad spectrum of changes found in AD are only seen, albeit to a lesser extent, in normal aging with other neurodegenerative diseases showing distinct spectrums of change. (C) 2002 Elsevier Science Inc.
引用
收藏
页码:1475 / 1479
页数:5
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