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Alzheimers Dement. 2014 May;10(3):393-400. doi: 10.1016/j.jalz.2013.04.508. Epub 2013 Jul 11.

Mitochondrial DNA deletions in Alzheimer's brains: a review.

Author information

1
Department of Forensic & Investigative Genetics, University of North Texas Health Science Center, Fort Worth, TX, USA. Electronic address: Nicole.Phillips@unthsc.edu.
2
Department of Physiology & Pharmacology, West Virginia University, Morgantown, WV, USA; Center for Basic and Translational Stroke Research, West Virginia University, Morgantown, WV, USA.
3
Department of Forensic & Investigative Genetics, University of North Texas Health Science Center, Fort Worth, TX, USA; Institute of Applied Genetics, University of North Texas Health Science Center, Fort Worth, TX, USA.

Abstract

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.

KEYWORDS:

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

PMID:
23850329
PMCID:
PMC3800237
DOI:
10.1016/j.jalz.2013.04.508
[Indexed for MEDLINE]
Free PMC Article

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