Mitochondrial aging and dysfunction in Alzheimer's disease

Patrick G. Sullivan, Maile R. Brown

Research output: Contribution to journalReview articlepeer-review

101 Scopus citations


Disruptions in energy metabolism have been suggested to be a prominent feature, perhaps even a fundamental component, of Alzheimer's disease (AD). These abnormalities in cerebral metabolism precede the onset of neurological dysfunction as well as gross neuropathology of AD. These changes may stem from inhibition of mitochondrial enzymes including pyruvate dehydrogenase, cytochrome c oxidase, and α-ketoglutarate dehydrogenase. Several lines of evidence also suggest a role for oxidative stress in the neuropathology associated with the disease state. Because mitochondria are the major site of free radical production in cells, they are also a primary target for oxidative damage and subsequent dysfunction. This link between mitochondrial dysfunction and the pathophysiology of AD is supported by several lines of evidence.

Original languageEnglish
Pages (from-to)407-410
Number of pages4
JournalProgress in Neuro-Psychopharmacology and Biological Psychiatry
Issue number3
StatePublished - Mar 2005


  • Alzheimer's disease
  • Brain aging
  • Mitochondria
  • Oxidative stress
  • Reactive oxygen species

ASJC Scopus subject areas

  • Pharmacology
  • Biological Psychiatry


Dive into the research topics of 'Mitochondrial aging and dysfunction in Alzheimer's disease'. Together they form a unique fingerprint.

Cite this