The roles of free radicals in amyotrophic lateral sclerosis

Danxia Liu

Research output: Contribution to journalArticle

29 Scopus citations

Abstract

The mutations of the Cu,Zn superoxide dismutase (Cu,Zn-SOD) gene observed in amyotrophic lateral sclerosis (ALS) patients suggest that free radicals play a role in this fatal disease. Free radicals trigger oxidative damage to proteins, membrane lipids, and DNA, thereby destroying neurons. Mutations of the SOD gene may reduce its superoxide dismutase activity, thereby elevating free radical levels. In addition, the mutant SOD protein may function as a peroxidase to oxidize cellular components, and it may also react with peroxynitrite - a product of the reaction between superoxide and nitric oxide - to ultimately form nitrate proteins. The selective degeneration of motor neurons in ALS may be caused by the high level of Cu,Zn-SOD present in and the large number of glutamatergic synapses projecting to these neurons. Free radical-triggered and age-accumulated oxidation may modify the program controlling motor neuron death, thereby initiating apoptosis of motor neurons in young adults.

Original languageEnglish (US)
Pages (from-to)159-167
Number of pages9
JournalJournal of Molecular Neuroscience
Volume7
Issue number3
DOIs
StatePublished - Jan 1 1996

Keywords

  • Amyotrophic lateral sclerosis
  • Cu,Zn superoxide dismutase
  • Free radicals
  • Glutamate toxicity
  • Motor neuron degeneration
  • Oxidative damage
  • Programmed neuron death

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

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