期刊
SCIENCE
卷 288, 期 5464, 页码 335-339出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.288.5464.335
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资金
- NINDS NIH HHS [R29 NS37345, P50 NS38370, R01 NS38586] Funding Source: Medline
Mutations in the copper/zinc superoxide dismutase (SOD1) gene produce an animal model of familiar amyotrophic Lateral sclerosis (ALS), a fatal neurodegenerative disorder., To test a new therapeutic strategy for ALS, we examined the effect of caspase inhibition in transgenic mice expressing mutant human SOD1 with a substitution of glycine to alanine in position 93 (mSOD1(G93A)). Intracerebroventricular administration of zVAD-fmk, a broad caspase inhibitor. delays disease onset and mortality. Moreover, zVAD-fmk inhibits caspase-1 activity as well as caspase-1 and caspase-3 mRNA up-regulation, providing evidence for a non-cell-autonomous pathway regulating caspase expression. Caspases play an instrumental role in neurodegeneration in transgenic mSOD1(G93A) mice, which suggests that caspase inhibition may have a protective role in ALS.
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