Oxidative stress and mitochondrial dysfunction in Alzheimer's disease

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE

卷:1842

Review

Wang, Xinglong¹  Wang, Wenzhang¹  Li, Li¹  Perry, George²  Lee, Hyoung-gon¹  Zhu, Xiongwei¹ 

[1] Case Western Reserve Univ, Dept Pathol, Cleveland, OH 44106 USA

[2] Univ Texas San Antonio, Dept Biol, San Antonio, TX USA

关键词: Alzheimer disease;    Oxidative stress;    Mitochondrial dysfunction;    Mitochondrial fission;    Mitochondrial fusion;    DLP1;   

DOI  :  10.1016/j.bbadis.2013.10.015

来源: Elsevier

【 摘 要 】

Alzheimer's disease (AD) exhibits extensive oxidative stress throughout the body, being detected peripherally as well as associated with the vulnerable regions of the brain affected in disease. Abundant evidence not only demonstrates the full spectrum of oxidative damage to neuronal macromolecules, but also reveals the occurrence of oxidative events early in the course of the disease and prior to the formation of the pathology, which support an important role of oxidative stress in AD. As a disease of abnormal aging, AD demonstrates oxidative damage at levels that significantly surpass that of elderly controls, which suggests the involvement of additional factor(s). Structurally and functionally damaged mitochondria, which are more proficient at producing reactive oxygen species but less so in ATP, are also an early and prominent feature of the disease. Since mitochondria are also vulnerable to oxidative stress, it is likely that a vicious downward spiral involving the interactions between mitochondrial dysfunction and oxidative stress contributes to the initiation and/or amplification of reactive oxygen species that is critical to the pathogenesis of AD. This article is part of a Special Issue entitled: Misfolded Proteins, Mitochondrial Dysfunction and Neurodegenerative Diseases. (C) 2013 Elsevier B.V. All rights reserved.

【 授权许可】

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