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DJ-1 Changes in G93A-SOD1 Transgenic Mice: Implications for Oxidative Stress in ALS

โœ Scribed by Nirit Lev; Debby Ickowicz; Yael Barhum; Eldad Melamed; Daniel Offen


Publisher
Humana Press Inc
Year
2008
Tongue
English
Weight
366 KB
Volume
38
Category
Article
ISSN
0895-8696

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## Abstract Amyotrophic lateral sclerosis (ALS) is caused by motor neuron loss in the spinal cord, but the mechanisms responsible are not known. Ubiquitous transgenic overexpression of copper/zinc superoxide dismutase (SOD1) mutations causing familial ALS (SOD1^mut^) leads to an ALS phenotype in mi

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Amyotrophic lateral sclerosis (ALS) is a fatal neurological disorder involving the selective degeneration of motor neurons. In a small proportion of patients, ALS is caused by mutations in copper/zinc superoxide dismutase (SOD1), and mice overexpressing SOD1 G93A mutant develop a syndrome that close