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J Mol Neurosci. 2011 Nov;45(3):445-52. doi: 10.1007/s12031-011-9588-1. Epub 2011 Jul 5.

c-Abl in neurodegenerative disease.

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  • 1Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, 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.

PMID:
21728062
PMCID:
PMC3329755
DOI:
10.1007/s12031-011-9588-1
[PubMed - indexed for MEDLINE]
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