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Neurology Research International
Volume 2011, Article ID 383087, 9 pages
Review Article

Animal Models of MS Reveal Multiple Roles of Microglia in Disease Pathogenesis

Program in Neurosciences, Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY 11794-8651, USA

Received 1 June 2011; Revised 5 September 2011; Accepted 5 September 2011

Academic Editor: Mamede de Carvalho

Copyright © 2011 Zhen Gao and Stella E. Tsirka. 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.


Multiple sclerosis (MS) is a progressive inflammatory and demyelinating disease that affects more than 2.5 million people worldwide every year. Current therapies use mostly disease-modifying drugs, focusing on blocking and regulating systemic functions and the central nervous system (CNS) infiltration of immune cells; however, these therapies only attenuate or delay MS symptoms, but are not effective in halting the disease progression. More recent evidence indicated that regulation of inflammation within the CNS might be a better way to approach the treatment of the disease and microglia, the resident immune cells, may be a promising target of therapeutic studies. Microglia activation classically accompanies MS development, and regulation of microglia function changes the outcome of the disease. In this paper, we review the contributions of microglia to MS pathogenesis and discuss microglial functions in antigen presentation, cytokine release, and phagocytosis. We describe data both from animal and human studies. The significant impact of the timing, intensity, and differentiation fate of activated microglia is discussed, as they can modulate MS outcomes and potentially be critically modified for future therapeutic studies.