Molecular targets for neuroprotection.
Amyotrophic lateral sclerosis (ALS) is a fatal paralytic neurodegenerative disorder. Experimental models of ALS such as the transgenic rodents expressing mutant superoxide dimutase-1 are playing a pivotal role in our understanding of ALS pathogenesis, and in our testing of new therapeutic interventions aimed at protecting against neurodegeneration. Apoptosis has emerged as a significant pathogenic factor in several neurodegenerative diseases, including ALS. Constructed of multiple interacting molecules, the apoptosis machinery offers a host of attractive targets for pharmacological and genetic interventions to be tested in experimental models of ALS. Information generated by these pre-clinical studies holds the promise to provide sound scientific basis for the development of effective neuroprotective therapies for ALS.
Przedborski
Serge
S
Departments of Neurology and Pathology, and the Center for Neurobiology and Behavior, Columbia University, New York, NY 10032, USA. SP30@columbia.edu
D000690:Amyotrophic Lateral Sclerosis / Q000188:drug therapy* / Q000235:genetics*; D000818:Animals; D017209:Apoptosis / Q000235:genetics; D020169:Caspases / Q000378:metabolism; D004195:Disease Models, Animal; D006801:Humans; D007249:Inflammation; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D010447:Peptide Hydrolases / Q000502:physiology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D013482:Superoxide Dismutase / Q000235:genetics; D000072105:Superoxide Dismutase-1
D018696:Neuroprotective Agents; D019253:Proto-Oncogene Proteins c-bcl-2; C000606290:SOD1 protein, human; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D010447:Peptide Hydrolases; D020169:Caspases