Mitochondria, Amyloid β, and Alzheimer's Disease
Joint Authors
Sullivan, Patrick G.
Readnower, Ryan D.
Sauerbeck, Andrew D.
Source
International Journal of Alzheimer's Disease
Issue
Vol. 2011, Issue 2011 (31 Dec. 2011), pp.1-5, 5 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2011-03-22
Country of Publication
Egypt
No. of Pages
5
Main Subjects
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.
American Psychological Association (APA)
Readnower, Ryan D.& Sauerbeck, Andrew D.& Sullivan, Patrick G.. 2011. Mitochondria, Amyloid β, and Alzheimer's Disease. International Journal of Alzheimer's Disease،Vol. 2011, no. 2011, pp.1-5.
https://search.emarefa.net/detail/BIM-446686
Modern Language Association (MLA)
Readnower, Ryan D.…[et al.]. Mitochondria, Amyloid β, and Alzheimer's Disease. International Journal of Alzheimer's Disease No. 2011 (2011), pp.1-5.
https://search.emarefa.net/detail/BIM-446686
American Medical Association (AMA)
Readnower, Ryan D.& Sauerbeck, Andrew D.& Sullivan, Patrick G.. Mitochondria, Amyloid β, and Alzheimer's Disease. International Journal of Alzheimer's Disease. 2011. Vol. 2011, no. 2011, pp.1-5.
https://search.emarefa.net/detail/BIM-446686
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-446686