title: ICE, neuronal apoptosis and neurodegeneration.
abstract: Significant progress has recently occurred in the understanding of the molecular mechanisms mediating vertebrate programmed cell death, or apoptosis. New advances in this field have stemmed from the identification of ICE (caspase-1) as the founding member of the mammalian caspase cell death family. Apoptotic cell death plays an important role in neuronal cell death. Both in vitro and in vivo evidence implicates ICE as an important factor in neuronal apoptosis, especially under pathological conditions. In addition, other caspases, such as caspase-3, have also been shown to be activated and may play a role in pathological neuronal loss. Understanding the basic mechanisms mediating cell death in neurodegenerative disease may lead to the development of novel approaches for the treatment of diseases featuring apoptosis.
authors: Neurosurgical Service, Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA.
authors: R M
authors: RM
authors: Friedlander
authors: J
authors: J
authors: Yuan
mesh_terms: D000818:Animals; D017209:Apoptosis; D001921:Brain / Q000473:pathology / Q000502:physiology / Q000503:physiopathology; D020170:Caspase 1 / Q000378:metabolism*; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism; D006801:Humans; D009410:Nerve Degeneration / Q000473:pathology / Q000503:physiopathology; D019636:Neurodegenerative Diseases / Q000473:pathology / Q000503:physiopathology*; D009474:Neurons / Q000166:cytology / Q000502:physiology*
chemical_list: C505407:CASP3 protein, human; D053148:Caspase 3; D020169:Caspases; D020170:Caspase 1