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International Journal of Alzheimer’s Disease
Volume 2012 (2012), Article ID 314185, 11 pages
http://dx.doi.org/10.1155/2012/314185
Review Article

Microglia in Alzheimer's Disease: It's All About Context

1Regenerative Medicine Institute Neural Program and Department of Biomedical Sciences, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Steven Spielberg Building Room 345, Los Angeles, CA 90048, USA
2Department of Neurosurgery, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Steven Spielberg Building Room 345, Los Angeles, CA 90048, USA
3Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90048, USA

Received 13 February 2012; Accepted 9 April 2012

Academic Editor: Colin Combs

Copyright © 2012 Tara M. Weitz and Terrence Town. 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.

Abstract

Neuroinflammation is now regarded as both an early event and prime mover in the pathobiology of Alzheimer disease (AD), a neurodegenerative disease that represents a growing public health threat. As the resident innate immune cells within the central nervous system, microglia are centrally positioned as key orchestrators of brain inflammation. It is now accepted that numerous forms of activated microglia exist. Furthermore, while some types of reactive microglia are detrimental, others can actually be beneficial. In the context of AD etiopathology, much debate surrounds whether these enigmatic cells play “good” or “bad” roles. In this article, we distill a complex clinical and experimental literature focused on the contribution of microglia to AD pathology and progression. A synthesis of the literature only seems possible when considering context– the conditions under which microglia encounter and mount immunological responses to AD pathology. In order to carry out these diverse contextual responses, a number of key receptors and signaling pathways are variously activated. It will be critically important for future studies to address molecular mediators that lead to beneficial microglial responses and therefore represent important therapeutic targets for AD.