Mitochondria, Amyloid β, and Alzheimer's Disease

Abstract EN

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.