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Parkinson’s Disease
Volume 2012, Article ID 271732, 8 pages
Review Article

Neuroinflammation in Parkinson's Disease and Related Disorders: A Lesson from Genetically Manipulated Mouse Models of -Synucleinopathies

1Division of Sensory and Motor Systems, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-0057, Japan
2Department of Physiology, Nippon Medical School, Tokyo 113-8602, Japan
3Division of Animal Sciences, National Institute of Agrobiological Sciences, Tsukuba, Ibaraki 305-8634, Japan

Received 7 December 2011; Accepted 18 January 2012

Academic Editor: Stephane Hunot

Copyright © 2012 Kazunari Sekiyama 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.


Neuroinflammation in Parkinson's disease (PD) is a chronic process that is associated with alteration of glial cells, including astrocytes and microglia. However, the precise mechanisms remain obscure. To better understand neuroinflammation in PD, we focused on glial activation in -synuclein ( S) transgenic and related model mice. In the majority of S transgenic mice, astrogliosis was observed concomitantly with accumulation of S during the early stage of neurodegeneration. However, microglia were not extensively activated unless the mice were treated with lipopolysaccharides or through further genetic modification of other molecules, including familial PD risk factors. Thus, the results in S transgenic mice and related model mice are consistent with the idea that neuroinflammation in PD is a double-edged sword that is protective in the early stage of neurodegeneration but becomes detrimental with disease progression.