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Functional Role of Caspase-1 and Caspase-3 in an ALS Transgenic Mouse Model
Abstract
Mutations in the copper/zinc superoxide dismutase (SOD1) gene produce an animal model of familial 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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Metadata
- Authors
- Li, M., Ona, V. O., Guégan, C., Chen, M., Jackson-Lewis, V., Andrews, L. J., Olszewski, A. J., Stieg, P. E., Lee, J.-P., Przedborski, S., & Friedlander, R. M.
- Venue
- Science
- Published
- 2000-04-14
- Volume
- 288
- Issue
- 5464
- Pages
- 335-339
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W1960735897
- Cited by
- 716
- References
- 1
- FWCI
- 42.68
- Type
- journal article
- Language
- en
- Open access
- closed
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