The role of cytochrome c oxidase deficiency in ROS and amyloid plaque formation

Alicia M. Pickrell, Hirokazu Fukui, Carlos T. Moraes

Research output: Contribution to journalShort surveypeer-review

33 Scopus citations


The multiple dysfunctional changes associated with a brain affected with Alzheimer's disease (AD) makes the understanding of primary pathogenic mechanisms challenging. Mitochondrial dysfunction has been associated with almost every neurodegenerative disease and neurodegenerative-related event. Alzheimer's disease is no exception with data suggesting mitochondrial malfunctions ranging from improper organelle dynamics, defective oxidative phosphorylation (OXPHOS), oxidative stress, and harmful beta amyloid (Aβ) associations with the mitochondria. A major change often associated with AD is impairment of the electron transport chain at complex IV: cytochrome c oxidase (COX). This mini-review concentrates on recent work by our group that sheds light on the role COX deficiency plays in the pathophysiology of AD using a transgenic mouse model. Results suggest that neuronal COX deficiency does not increase oxidative stress and nor increases amyloidal formations in vivo. Conclusions from this work also suggest that Aβ formation is a cause of COX deficiency as opposed to the consequence.

Original languageEnglish (US)
Pages (from-to)453-456
Number of pages4
JournalJournal of Bioenergetics and Biomembranes
Issue number5
StatePublished - Oct 2009


  • Alzheimer's disease
  • Amyloid formation
  • COX deficiency
  • Oxidative stress

ASJC Scopus subject areas

  • Physiology
  • Cell Biology


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