title: c-Abl in neurodegenerative disease.
abstract: The c-Abl tyrosine kinase participates in a variety of cellular functions, including regulation of the actin cytoskeleton, regulation of the cell cycle, and the apoptotic/cell cycle arrest response to stress, and the Abl family of kinases has been shown to play a crucial role in development of the central nervous system. Recent studies have shown c-Abl activation in human Alzheimer's and Parkinson's diseases and c-Abl activation in mouse models and neuronal culture in response to amyloid beta fibrils and oxidative stress. Overexpression of active c-Abl in adult mouse neurons results in neurodegeneration and neuroinflammation. Based on this evidence, a potential role for c-Abl in the pathogenesis of neurodegenerative disease is discussed, and we attempt to place activation of c-Abl in context with other known contributors to neurodegenerative pathology.
authors: Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
authors: Sarah D
authors: SD
authors: Schlatterer
authors: Christopher M
authors: CM
authors: Acker
authors: Peter
authors: P
authors: Davies
mesh_terms: D000544:Alzheimer Disease / Q000201:enzymology / Q000473:pathology; D000818:Animals; D004249:DNA Damage; D004660:Encephalitis / Q000378:metabolism / Q000473:pathology; D004789:Enzyme Activation; D006801:Humans; D019636:Neurodegenerative Diseases / Q000201:enzymology* / Q000235:genetics / Q000473:pathology; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress; D016315:Proto-Oncogene Proteins c-abl / Q000235:genetics / Q000378:metabolism*; D016875:tau Proteins / Q000378:metabolism
chemical_list: D016875:tau Proteins; D016315:Proto-Oncogene Proteins c-abl