Decreased glutathione accelerates neurological deficit and mitochondrial pathology in familial ALS-linked hSOD1G93A mice model

Dominant mutations in Cu/Zn-superoxide dismutase (SOD1) cause familial forms of amyotrophic lateral sclerosis (ALS), a fatal disorder characterized by the progressive loss of motor neurons. To investigate the role of antioxidant defenses in ALS we used knockout mice for the glutamate-cysteine ligase...

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Bibliografiska uppgifter

Huvudupphov:	Marcelo R. Vargas, Delinda A. Johnson, Jeffrey A. Johnson
Materialtyp:	Artigo
Språk:	Inglês
Utgiven:	Elsevier 2011-09-01
Serie:	Neurobiology of Disease
Ämnen:	Amyotrophic lateral sclerosis Glutathione GCLM Mitochondria
Länkar:	http://www.sciencedirect.com/science/article/pii/S0969996111001422
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