Journal of Molecular Neuroscience

, Volume 45, Issue 3, pp 445–452

c-Abl in Neurodegenerative Disease

  • Sarah D. Schlatterer
  • Christopher M. Acker
  • Peter Davies
Article

DOI: 10.1007/s12031-011-9588-1

Cite this article as:
Schlatterer, S.D., Acker, C.M. & Davies, P. J Mol Neurosci (2011) 45: 445. doi:10.1007/s12031-011-9588-1

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.

Keywords

Tau Alzheimer’s c-Abl Tyrosine kinase Tauopathy 

Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  • Sarah D. Schlatterer
    • 1
  • Christopher M. Acker
    • 1
  • Peter Davies
    • 1
    • 2
  1. 1.Department of PathologyAlbert Einstein College of MedicineBronxUSA
  2. 2.Litwin-Zucker Center for Research in Alzheimer’s Disease and Memory Disorders, Feinstein Center for Medical Research, North ShoreLong Island Jewish Health SystemManhassetUSA

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