Mitochondrial dysfunction and oxidative damage in Alzheimer's and Parkinson's diseases and coenzyme Q10 as a potential treatment

J Bioenerg Biomembr. 2004 Aug;36(4):381-6. doi: 10.1023/B:JOBB.0000041772.74810.92.

Abstract

There is substantial evidence that mitochondrial dysfunction and oxidative damage may play a key role in the pathogenesis of neurodegenerative disease. Evidence supporting this in both Alzheimer's and Parkinson's diseases is continuing to accumulate. This review discusses the increasing evidence for a role of both mitochondrial dysfunction and oxidative damage in contributing to beta-amyloid deposition in Alzheimer's disease. I also discuss the increasing evidence that Parkinson's disease is associated with abnormalities in the electron transport gene as well as oxidative damage. Lastly, I reviewed the potential efficacy of coenzyme Q as well as a number of other antioxidants in the treatment of both Parkinson's and Alzheimer's diseases.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Alzheimer Disease / complications
  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / metabolism*
  • Amyloid beta-Peptides / metabolism*
  • Animals
  • Brain / drug effects
  • Brain / metabolism
  • Coenzymes
  • Humans
  • Mitochondria / drug effects
  • Mitochondria / metabolism*
  • Mitochondrial Diseases / complications
  • Mitochondrial Diseases / drug therapy
  • Mitochondrial Diseases / metabolism*
  • Neurons / metabolism
  • Neuroprotective Agents / therapeutic use
  • Oxidation-Reduction
  • Oxidative Stress / drug effects
  • Parkinson Disease / drug therapy*
  • Parkinson Disease / metabolism*
  • Reactive Oxygen Species / metabolism
  • Ubiquinone / analogs & derivatives*
  • Ubiquinone / therapeutic use*

Substances

  • Amyloid beta-Peptides
  • Coenzymes
  • Neuroprotective Agents
  • Reactive Oxygen Species
  • Ubiquinone
  • coenzyme Q10