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c-Abl in neurodegenerative disease
Authors:Schlatterer Sarah D  Acker Christopher M  Davies Peter
Affiliation:1. Department of Pathology, Albert Einstein College of Medicine, Bronx, NY, 10461, USA
2. Litwin-Zucker Center for Research in Alzheimer’s Disease and Memory Disorders, Feinstein Center for Medical Research, North Shore, Long Island Jewish Health System, Manhasset, NY, 11030, USA
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.
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