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International Journal of Alzheimer’s Disease
Volume 2011 (2011), Article ID 129753, 9 pages
Review Article

Glycogen Synthase Kinase-3β: A Mediator of Inflammation in Alzheimer's Disease?

1Department of Neurobiology, A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland
2Department of Oncology, Kuopio University Hospital, P.O. Box 1777, 70211 Kuopio, Finland

Received 7 February 2011; Accepted 4 March 2011

Academic Editor: Peter Crouch

Copyright © 2011 Jari Koistinaho 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.


Proliferation and activation of microglial cells is a neuropathological characteristic of brain injury and neurodegeneration, including Alzheimer's disease. Microglia act as the first and main form of immune defense in the nervous system. While the primary function of microglia is to survey and maintain the cellular environment optimal for neurons in the brain parenchyma by actively scavenging the brain for damaged brain cells and foreign proteins or particles, sustained activation of microglia may result in high production of proinflammatory mediators that disturb normal brain functions and even cause neuronal injury. Glycogen synthase kinase-3β has been recently identified as a major regulator of immune system and mediates inflammatory responses in microglia. Glycogen synthase kinase-3β has been extensively investigated in connection to tau and amyloid β toxicity, whereas reports on the role of this enzyme in neuroinflammation in Alzheimer's disease are negligible. Here we review and discuss the role of glycogen synthase-3β in immune cells in the context of Alzheimer's disease pathology.