Mitochondrial DNA deletions in Alzheimer's brains: A review

被引:44
作者
Phillips, Nicole R. [1 ]
Simpkins, James W. [3 ,4 ]
Roby, Rhonda K. [1 ,2 ]
机构
[1] Univ N Texas, Hlth Sci Ctr, Dept Forens & Invest Genet, Ft Worth, TX 76129 USA
[2] Univ N Texas, Hlth Sci Ctr, Inst Appl Genet, Ft Worth, TX USA
[3] W Virginia Univ, Dept Physiol & Pharmacol, Morgantown, WV 26506 USA
[4] W Virginia Univ, Ctr Basic & Translat Stroke Res, Morgantown, WV 26506 USA
关键词
Alzheimer's disease; Mitochondrial DNA deletion; DNA damage; Oxidative stress; Neurodegeneration; LARGE-SCALE DELETIONS; KEARNS-SAYRE SYNDROME; CLONAL EXPANSION; REACTIVE OXYGEN; NUCLEAR-DNA; DISEASE; DAMAGE; NEURONS; REPAIR; HETEROGENEITY;
D O I
10.1016/j.jalz.2013.04.508
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Mitochondrial dysfunction and increased oxidative stress have been associated with normal aging and are possibly implicated in the etiology of late-onset Alzheimer's disease (AD). DNA deletions, as well as other alterations, can result from oxidative damage to nucleic acids. Many studies during the past two decades have investigated the incidence of mitochondrial DNA deletions in postmortem brain tissues of late-onset AD patients compared with age-matched normal control subjects. Published studies are not entirely concordant, but their differences might shed light on the heterogeneity of AD itself. Our understanding of the role that mitochondrial DNA deletions play in disease progression may provide valuable information that could someday lead to a treatment. (C) 2014 The Alzheimer's Association. All rights reserved.
引用
收藏
页码:393 / 400
页数:8
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