title: Mitochondria, Amyloid β, and Alzheimer's Disease.
abstract: 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, Aβ has been shown to directly inhibit mitochondrial enzymes. Inhibition of mitochondrial enzymes as a result of oxidative damage or Aβ 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.
authors.affiliation: Spinal Cord & Brain Injury Research Center, University of Kentucky, Lexington, KY 40536, USA.
authors.forename: Ryan D
authors.initials: RD
authors.lastname: Readnower
authors.forename: Andrew D
authors.initials: AD
authors.lastname: Sauerbeck
authors.forename: Patrick G
authors.initials: PG
authors.lastname: Sullivan