Oxidative stress and mitochondrial dysfunction in neurodegenerative diseases

Eugenia D Trushina, C. T. McMurray

Research output: Contribution to journalArticle

283 Citations (Scopus)

Abstract

In recent years, it has become increasingly clear that mitochondrial dysfunction and oxidative damage are major contributors to neuronal loss. Free radicals, typically generated from mitochondrial respiration, cause oxidative damage of nucleic acids, lipids, carbohydrates and proteins. Despite enormous amount of effort, however, the mechanism by which oxidative damage causes neuronal death is not well understood. Emerging data from a number of neurodegenerative diseases suggest that there may be common features of toxicity that are related to oxidative damage. In this review, while focusing on Huntington's disease (HD), we discuss similarities among HD, Friedreich ataxia and xeroderma pigmentosum, which provide insight into shared mechanisms of neuronal death.

Original languageEnglish (US)
Pages (from-to)1233-1248
Number of pages16
JournalNeuroscience
Volume145
Issue number4
DOIs
StatePublished - Apr 14 2007

Fingerprint

Huntington Disease
Neurodegenerative Diseases
Oxidative Stress
Friedreich Ataxia
Xeroderma Pigmentosum
Nucleic Acids
Free Radicals
Cause of Death
Respiration
Carbohydrates
Lipids
Proteins

Keywords

  • Friedreich ataxia
  • Huntington's disease
  • mitochondria
  • neurodegeneration
  • oxidative damage
  • xeroderma pigmentosum

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Oxidative stress and mitochondrial dysfunction in neurodegenerative diseases. / Trushina, Eugenia D; McMurray, C. T.

In: Neuroscience, Vol. 145, No. 4, 14.04.2007, p. 1233-1248.

Research output: Contribution to journalArticle

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