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Science 14 April 2000:
Vol. 288. no. 5464, pp. 335 - 339
DOI: 10.1126/science.288.5464.335
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Reports

Functional Role of Caspase-1 and Caspase-3 in an ALS Transgenic Mouse Model

Mingwei Li, 1 Victor O. Ona, 1 Christelle Guégan, 2 Minghua Chen, 1 Vernice Jackson-Lewis, 2 L. John Andrews, 1 Adam J. Olszewski, 1 Philip E. Stieg, 1 Jean-Pyo. Lee, 4 Serge Przedborski, 23 Robert M. Friedlander 1*

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 (mSOD1G93A). 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 mSOD1G93A mice, which suggests that caspase inhibition may have a protective role in ALS.

1 Neuroapoptosis Laboratory and Neurosurgical Service, Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
2 Department of Neurology,
3 Department of Pathology, Columbia University, New York, NY 10032, USA.
4 Department of Medicine, University of Chicago, Chicago, IL 60637, USA.
*   To whom correspondence should be addressed. E-mail: rfriedlander{at}rics.bwh.harvard.edu

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