Journal
FREE RADICAL BIOLOGY AND MEDICINE
Volume 43, Issue 12, Pages 1569-1573Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2007.09.007
Keywords
Alzheimer disease; fission; fusion; mitochondria; oxidative stress; free radicals
Funding
- NIA NIH HHS [AG026151, AG024028] Funding Source: Medline
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Arnyloid-beta has long been implicated in the pathogenesis of Alzheimer disease. The focus was initially on the extracellular fibrillar deposits of amyloid-beta but more recently has shifted to intracellular oligomeric forms of amyloid-P. Unfortunately, the mechanism(s) by which either extracellular or intracellular amyloid-beta induces neuronal toxicity remains unclear. That said, a number of recent studies indicate that mitochondria might be an important target of amyloid-beta. Neurons rely heavily on mitochondria for energy and it is well established that mitochondrial dysfunction might be an important target of amyloid-beta. Mechanistically, amyloid-beta aggregates in mitochondria to impair function, leading to energy hypometabolism and elevated reactive oxygen species production. Additionally, arnyloid-beta affects the balance of mitochondrial fission/ fusion and mitochondrial transport, negatively impacting a host of cellular functions of neurons. Here, we review the role that amyloid-beta plays in mitochondrial structure and function of neurons and the importance of this in the pathogenesis of Alzheimer disease. (C) 2007 Elsevier Inc. All rights reserved.
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