Mitochondria, amyloid β, and Alzheimer's disease

Patrick G. Sullivan, Ryan D. Readnower, Andrew D. Sauerbeck

Research output: Contribution to journalReview articlepeer-review

51 Scopus citations


Hypometabolism is a hallmark of Alzheimer's disease (AD) and implicates a mitochondrial role in the neuropathology associated with AD. Mitochondrial amyloid-beta (Aβ) accumulation precedes extracellular Aβ deposition. In addition to increasing oxidative stress, A has been shown to directly inhibit mitochondrial enzymes. Inhibition of mitochondrial enzymes as a result of oxidative damage or A interaction perpetuates oxidative stress and leads to a hypometabolic state. Additionally, Aβ has also been shown to interact with cyclophilin D, a component of the mitochondrial permeability transition pore, which may promote cell death. Therefore, ample evidence exists indicating that the mitochondrion plays a vital role in the pathophysiology observed in AD.

Original languageEnglish
Article number104545
JournalInternational Journal of Alzheimer's Disease
StatePublished - 2011

ASJC Scopus subject areas

  • Aging
  • Neurology
  • Clinical Neurology
  • Cognitive Neuroscience
  • Cellular and Molecular Neuroscience
  • Behavioral Neuroscience


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