Brain iron deposition and the free radical-mitochondrial theory of ageing

被引：213

作者：

Schipper, HM ^{[1
]}

机构：

[1] McGill Univ, Sir Mortimer B Davis Jewish Hosp, Lady Davis Inst Med Res, Ctr Neurotranslat Res, Montreal, PQ H3T 1E2, Canada

[2] McGill Univ, Sir Mortimer B Davis Jewish Hosp, Lady Davis Inst Med Res, Bloomfield Ctr Res Ageing, Montreal, PQ H3T 1E2, Canada

来源：

AGEING RESEARCH REVIEWS | 2004年 / 3卷 / 03期

基金：

加拿大健康研究院;

关键词：

ageing; heme oxygenase-1; iron; mitochondria; neurodegeneration; oxidative stress;

D O I：

10.1016/j.arr.2004.02.001

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 [细胞生物学]; 090102 [作物遗传育种];

摘要：

The central hypothesis of this paper states that oxidative stress, augmented iron deposition, and mitochondrial insufficiency in the ageing and degenerating CNS constitute a single neuropathological 'lesion', and that the advent of one component of this triad obligates the appearance of the others. Evidence in support of this unifying perspective is adduced from human neuropathological studies, experimental paradigms of ageing-associated neurological disorders, and a comprehensive model of astroglial senescence. A pivotal role for the enzyme, heme oxygenase-1 (HO-1) in consolidating this tripartite lesion in the ageing and diseased CNS is emphasized. The data are discussed in the context of a revised 'free radical-mitochondrial-metal' theory of brain ageing, and some scientific and clinical implications of the latter are considered. (C) 2004 Elsevier Ireland Ltd. All rights reserved.

引用

页码：265 / 301

页数：37

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