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Biochim Biophys Acta. 2014 Aug;1842(8):1240-7. doi: 10.1016/j.bbadis.2013.10.015. Epub 2013 Nov 1.

Oxidative stress and mitochondrial dysfunction in Alzheimer's disease.

Author information

1
Department of Pathology, Case Western Reserve University, Cleveland, OH, USA. Electronic address: xinglong.wang@case.edu.
2
Department of Pathology, Case Western Reserve University, Cleveland, OH, USA.
3
Department of Biology, The University of Texas at San Antonio, San Antonio, TX, USA.
4
Department of Pathology, Case Western Reserve University, Cleveland, OH, USA. Electronic address: xiongwei.zhu@case.edu.

Abstract

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.

KEYWORDS:

Alzheimer disease; DLP1; Mitochondrial dysfunction; Mitochondrial fission; Mitochondrial fusion; Oxidative stress

PMID:
24189435
PMCID:
PMC4007397
DOI:
10.1016/j.bbadis.2013.10.015
[Indexed for MEDLINE]
Free PMC Article

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