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Mitochondrial DNA deletions in Alzheimer's brains: A review

Journal

ALZHEIMERS & DEMENTIA
Volume 10, Issue 3, Pages 393-400

Publisher

WILEY
DOI: 10.1016/j.jalz.2013.04.508

Keywords

Alzheimer's disease; Mitochondrial DNA deletion; DNA damage; Oxidative stress; Neurodegeneration

Funding

  1. National Institute of Aging, Training in the Neurobiology of Aging [T32 AG 020494]

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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.

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