Mitochondria, Amyloid β, and Alzheimer's Disease

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 inh...

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Bibliographic Details
Published in:International journal of alzheimer's disease 2011, Vol.2011 (2011), p.1-5
Main Authors: Readnower, Ryan D., Sullivan, Patrick G., Sauerbeck, Andrew D.
Format: Article
Language:English
Subjects:
Alzheimer's disease
Amyloid beta-protein
Development and progression
Mitochondria
Physiological aspects
Review
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Summary: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.
ISSN:2090-8024
2090-0252
2090-0252
DOI:10.4061/2011/104545