Alzheimer's disease: Diverse aspects of mitochondrial malfunctioning

Renato X. Santos, Sónia C. Correia, Xinglong Wang, George Perry, Mark A. Smith, Paula I. Moreira, Xiongwei Zhu

Research output: Contribution to journalArticlepeer-review

90 Scopus citations

Abstract

Alzheimer's disease is a progressive neurodegenerative disorder, either assuming a sporadic, ageassociated, late-onset form, or a familial form, with early onset, in a smaller fraction of the cases. Whereas in the familial cases several mutations have been identified in genes encoding proteins related with the pathogenesis of the disease, for the sporadic form several causes have been proposed and are currently under debate. Mitochondrial dysfunction has surfaced as one of the most discussed hypotheses acting as a trigger for the pathogenesis of Alzheimer's disease. Mitochondria assume central functions in the cell, including ATP production, calcium homeostasis, reactive oxygen species generation, and apoptotic signaling. Although their role as the cause of the disease may be controversial, there is no doubt that mitochondrial dysfunction, abnormal mitochondrial dynamics and degradation by mitophagy occur during the disease process, contributing to its onset and progression.

Original languageEnglish (US)
Pages (from-to)570-581
Number of pages12
JournalInternational Journal of Clinical and Experimental Pathology
Volume3
Issue number6
StatePublished - 2010
Externally publishedYes

Keywords

  • Alzheimer's disease
  • Mitochondria
  • Mitochondrial dynamics
  • Mitochondrial dysfunction

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Histology

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