Delaying Caspase Activation by Bcl-2: A Clue to Disease Retardation in a Transgenic Mouse Model of Amyotrophic Lateral Sclerosis

This study is supported by Muscular Dystrophy Association, the Amyotrophic Lateral Sclerosis (ALS) Association, Project-ALS, the National Institute of Neurological Disorders and Stroke (Grants R01 NS38586, R29 NS37345, P50 NS38370), the United States Department of Defense (Grant DAMD 17-99-1-9471), the Lowenstein Foundation, the Smart Foundation, and the Parkinson's Disease Foundation. L.S. is a recipient of the Burroughs Wellcome Career Award in Biomedical Sciences, and C.G. is a recipient of a scholarship from the Institut National de la Santé et de la Recherche Médicale (France). We are grateful to Drs. A. Srinivasan (Idun Pharmaceutical, La Jolla, CA) for providing the CM1 antibody, G. M. Cole (UCLA, Los Angeles, CA) for providing the fractin antibody, and P. Pasinelli for insightful comments on this manuscript.

Correspondence should be addressed to Dr. Serge Przedborski, Departments of Neurology and Pathology, BB-307, Columbia University, 650 West 168th Street, New York, NY 10032. E-mail: SP30{at}Columbia.edu.