Mitochondrial amyloid-beta peptide: Pathogenesis or late-phase development?

Du Yan Shi, Wen Cheng Xiong, David M. Stern

Research output: Contribution to journalReview articlepeer-review

16 Scopus citations

Abstract

Mitochondrial and metabolic dysfunction have been linked to Alzheimer's disease for some time. Key questions regarding this association concern the nature and mechanisms of mitochondrial dysfunction, and whether such changes in metabolic properties are pathogenic or secondary, with respect to neuronal degeneration. In terms of mitochondria and Alzheimer's, altered function could reflect intrinsic properties of this organelle, potentially due to mutations in mitochondrial DNA, or extrinsic changes secondary to signal transduction mechanisms activated in the cytosol. This review presents data relevant to these questions, and considers the implication of recent findings demonstrating the presence of amyloid-β peptide in mitochondria, as well as intra-mitochondrial molecular targets with which it can interact. Regardless of the underlying mechanism(s), it is likely that mitochondrial dysfunction contributes to oxidant stress which is commonly observed in brains of patients with Alzheimer's and transgenic models of Alzheimer's-like pathology.

Original languageEnglish (US)
Pages (from-to)127-137
Number of pages11
JournalJournal of Alzheimer's Disease
Volume9
Issue number2
DOIs
StatePublished - 2006

Keywords

  • Alzheimer's disease
  • Apoptosis
  • Neurodegeneration
  • Reactive oxygen species
  • Respiratory chain complex

ASJC Scopus subject areas

  • Neuroscience(all)
  • Clinical Psychology
  • Geriatrics and Gerontology
  • Psychiatry and Mental health

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