Oxidative Stress Signaling in Alzheimer's Disease

被引:232
作者
Su, B. [1 ]
Wang, X. [1 ]
Nunomura, A. [2 ]
Moreira, P. I. [3 ]
Lee, H. -gon [1 ]
Perry, G. [1 ,4 ]
Smith, M. A. [1 ]
Zhu, X. [1 ]
机构
[1] Case Western Reserve Univ, Dept Pathol, Cleveland, OH 44106 USA
[2] Univ Yamanashi, Interdisciplinary Grad Sch Med & Engn, Dept Neuropsychiat, Yamanashi, Japan
[3] Univ Coimbra, Ctr Neurosci & Cell Biol Coimbra, Coimbra, Portugal
[4] Univ Texas San Antonio, Coll Sci, San Antonio, TX USA
基金
美国国家卫生研究院;
关键词
Alzheimer disease; compensation; JNK pathway; oxidative stress; signal transduction;
D O I
10.2174/156720508786898451
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Multiple lines of evidence demonstrate that oxidative stress is an early event in Alzheimer's disease (AD), occurring prior to cytopathology, and therefore may play a key pathogenic role in AD. Oxidative stress not only temporally precedes the pathological lesions of the disease but also activates cell signaling pathways, which, in turn, contribute to lesion formation and, at the same time, provoke cellular responses such as compensatory upregulation of antioxidant enzymes found in vulnerable neurons in AD. In this review, we provide an overview of the evidence of oxidative stress and compensatory responses that occur in AD, particularly focused on potential sources of oxidative stress and the roles and mechanism of activation of stress-activated protein kinase pathways.
引用
收藏
页码:525 / 532
页数:8
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