Journal of Molecular Neuroscience

, Volume 45, Issue 3, pp 445-452

First online:

c-Abl in Neurodegenerative Disease

  • Sarah D. SchlattererAffiliated withDepartment of Pathology, Albert Einstein College of Medicine
  • , Christopher M. AckerAffiliated withDepartment of Pathology, Albert Einstein College of Medicine
  • , Peter DaviesAffiliated withDepartment of Pathology, Albert Einstein College of MedicineLitwin-Zucker Center for Research in Alzheimer’s Disease and Memory Disorders, Feinstein Center for Medical Research, North Shore, Long Island Jewish Health System Email author 

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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.


Tau Alzheimer’s c-Abl Tyrosine kinase Tauopathy