Mitochondrial DNA deletions in Alzheimer's brains: a review

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


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Alzheimer Disease / genetics*
  • Alzheimer Disease / metabolism*
  • Animals
  • Brain / metabolism*
  • DNA, Mitochondrial*
  • Humans
  • Sequence Deletion*


  • DNA, Mitochondrial