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International Journal of Alzheimer’s Disease
Volume 2012, Article ID 276803, 4 pages
Review Article

Glycogen Synthase Kinase 3: A Point of Integration in Alzheimer's Disease and a Therapeutic Target?

1Department of Psychiatry, Douglas Hospital Research Center, McGill University, Montreal, QC, Canada H4H 1R3
2UTSA Neurosciences Institute and Department of Biology, College of Sciences, The University of Texas at San Antonio, San Antonio, TX, USA
3Department of Pathology, Case Western Reserve University, Cleveland, OH, USA
4Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal
5Faculty of Medicine, Institute of Physiology, University of Coimbra, Coimbra, Portugal

Received 7 February 2012; Revised 20 April 2012; Accepted 3 May 2012

Academic Editor: Francesco Panza

Copyright © 2012 Siddhartha Mondragón-Rodríguez 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 (GSK3) has been implicated in neurological disorders; therefore, it is not surprising that there has been an increased focus towards developing therapies directed to this kinase. Unfortunately, these current therapies have not taken into consideration the physiological role of GSK3 in crucial events like synaptic plasticity. With this in mind we will discuss the relationship of synaptic plasticity with GSK3 and tau protein and their role as potential targets for the development of therapeutic strategies. Finally, we will provide perspectives in developing a cocktail therapy for Alzheimer's treatment.