Mitochondrial dysfunction and Alzheimer's disease

Prog Neuropsychopharmacol Biol Psychiatry. 2011 Mar 30;35(2):320-30. doi: 10.1016/j.pnpbp.2010.07.004. Epub 2010 Jul 16.


To date, one of the most discussed hypotheses for Alzheimer's disease (AD) etiology implicates mitochondrial dysfunction and oxidative stress as one of the primary events in the course of AD. In this review we focus on the role of mitochondria and mitochondrial DNA (mtDNA) variation in AD and discuss the rationale for the involvement of mitochondrial abnormalities in AD pathology. We summarize the current data regarding the proteins involved in mitochondrial function and pathology observed in AD, and discuss the role of somatic mutations and mitochondrial haplogroups in AD development.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Alzheimer Disease / genetics
  • Alzheimer Disease / metabolism*
  • Alzheimer Disease / pathology
  • Amyloid beta-Peptides / metabolism*
  • Amyloid beta-Protein Precursor / metabolism*
  • Animals
  • Apolipoprotein E4 / genetics
  • Apolipoprotein E4 / metabolism*
  • Brain / metabolism
  • Brain / pathology
  • DNA, Mitochondrial / genetics
  • DNA, Mitochondrial / metabolism
  • Humans
  • Mitochondria / genetics
  • Mitochondria / metabolism*
  • Mitochondria / pathology
  • Oxidative Stress*


  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor
  • Apolipoprotein E4
  • DNA, Mitochondrial