Mitochondrial DNA deletions in Alzheimer's brains: A review

Nicole R. Phillips, James W. Simpkins, Rhonda K. Roby

Research output: Contribution to journalReview articlepeer-review

41 Scopus citations


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.

Original languageEnglish
Pages (from-to)393-400
Number of pages8
JournalAlzheimer's and Dementia
Issue number3
StatePublished - May 2014


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


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