Insights into amyloid-β-induced mitochondrial dysfunction in Alzheimer disease

Xinglong Wang, Bo Su, George Perry, Mark A. Smith, Xiongwei Zhu

Research output: Contribution to journalReview articlepeer-review

Abstract

Amyloid-β has long been implicated in the pathogenesis of Alzheimer disease. The focus was initially on the extracellular fibrillar deposits of amyloid-β but more recently has shifted to intracellular oligomeric forms of amyloid-β. Unfortunately, the mechanism(s) by which either extracellular or intracellular amyloid-β induces neuronal toxicity remains unclear. That said, a number of recent studies indicate that mitochondria might be an important target of amyloid-β. Neurons rely heavily on mitochondria for energy and it is well established that mitochondrial dysfunction might be an important target of amyloid-β. Mechanistically, amyloid-β aggregates in mitochondria to impair function, leading to energy hypometabolism and elevated reactive oxygen species production. Additionally, amyloid-β 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-β plays in mitochondrial structure and function of neurons and the importance of this in the pathogenesis of Alzheimer disease.

Original languageEnglish (US)
Pages (from-to)1569-1573
Number of pages5
JournalFree Radical Biology and Medicine
Volume43
Issue number12
DOIs
StatePublished - Dec 15 2007
Externally publishedYes

Keywords

  • Alzheimer disease
  • Fission
  • Free radicals
  • Fusion
  • Mitochondria
  • Oxidative stress

ASJC Scopus subject areas

  • Biochemistry
  • Physiology (medical)

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