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International Journal of Alzheimer’s Disease
Volume 2011, Article ID 189246, 9 pages
Review Article

GSK-3 in Neurodegenerative Diseases

1Mental Health Research Institute, 155 Oak Street, Parkville, VIC 3052, Australia
2Department of Pathology, The University of Melbourne, Carlton, VIC 3010, Australia
3Center for Neuroscience, The University of Melbourne, Carlton, VIC 3010, Australia

Received 27 January 2011; Accepted 7 March 2011

Academic Editor: Peter Crouch

Copyright © 2011 Peng Lei et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Glycogen synthase kinase-3 (GSK-3) regulates multiple cellular processes, and its dysregulation is implicated in the pathogenesis of diverse diseases. In this paper we will focus on the dysfunction of GSK-3 in Alzheimer’s disease and Parkinson’s disease. Specifically, GSK-3 is known to interact with tau, β-amyloid (Aβ), and α-synuclein, and as such may be crucially involved in both diseases. Aβ production, for example, is regulated by GSK-3, and its toxicity is mediated by GSK-induced tau phosphorylation and degeneration. α-synuclein is a substrate for GSK-3 and GSK-3 inhibition protects against Parkinsonian toxins. Lithium, a GSK-3 inhibitor, has also been shown to affect tau, Aβ, and α-synuclein in cell culture, and transgenic animal models. Thus, understanding the role of GSK-3 in neurodegenerative diseases will enhance our understanding of the basic mechanisms underlying the pathogenesis of these disorders and also facilitate the identification of new therapeutic avenues.