Home LiteratureArticle Details
PMID: 11881740 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S. Review

Superoxide dismutase and the death of motoneurons in ALS.

Trends in neurosciences ·Vol. 24 ·No. 11 Suppl ·2001-11-00 ·Pages S15-20

Beckman JS, Estévez AG, Crow JP, Barbeito L

Abstract

Amyotrophic lateral sclerosis (ALS) is a lethal disease that is characterized by the relentless death of motoneurons. Mutations to Cu-Zn superoxide dismutase (SOD), though occurring in just 2-3% of individuals with ALS, remain the only proven cause of the disease. These mutations structurally weaken SOD, which indirectly decreases its affinity for Zn. Zn-deficient SOD induces apoptosis in motoneurons through a mechanism involving peroxynitrite. Importantly, Zn-deficient wild-type SOD is just as toxic as Zn-deficient ALS mutant SOD, suggesting that the loss of Zn from wild-type SOD could be involved in the other 98% of cases of ALS. Zn-deficient SOD could therefore be an important therapeutic target in all forms of ALS.

MeSH Terms
Amyotrophic Lateral Sclerosis/metabolism,pathology Cell Death Humans Motor Neurons/enzymology,pathology Superoxide Dismutase/metabolism
Chemicals
Superoxide Dismutase
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Beckman J S
Linus Pauling Institute, and Dept of Biochemistry and Biophysics, Oregon State University, Corvallis 97331, USA. joe.beckman@orst.edu
Estévez A G
Crow J P
Barbeito L
Article Info
Journal
Trends in neurosciences
Abbr.
Trends Neurosci
ISSN
0166-2236
Published
2001-11-00
Pages
S15-20
Language
English
Region
England
NLM ID
7808616
Subset
IM
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