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Mediators of Inflammation
Volume 2012, Article ID 401264, 12 pages
Review Article

Oxidative Stress and Microglial Cells in Parkinson's Disease

North Carolina Oral Health Institute, The University of North Carolina at Chapel Hill, CB#7454, Chapel Hill, NC 27599-7454, USA

Received 4 November 2011; Revised 3 January 2012; Accepted 9 January 2012

Academic Editor: Luc Vallières

Copyright © 2012 Lynda J. Peterson and Patrick M. Flood. 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.


Significant evidence has now been accumulated that microglial cells play a central role in the degeneration of DA neurons in animal models of PD. The oxidative stress response by microglial cells, most notably the activity of the enzyme NADPH oxidase, appears to play a central role in the pathology of PD. This oxidative stress response occurs in microglia through the activation of the ERK signaling pathway by proinflammatory stimuli, leading to the phosphorylation and translocation of the p47phox and p67phox cytosolic subunits, the activation of membrane-bound PHOX, and the production of ROS. Therapeutic anti-inflammatories which prevent DA neurodegeneration in PD, including anti-inflammatory cytokines, morphinan compounds, NADPH oxidase inhibitors, NF-κB inhibitors, and β2-AR agonists, all function to inhibit the activation of the PHOX in microglial cells. These observations suggest a central role for the oxidative stress response in microglial cells as a mediator or regulator of DA neurodegeneration in PD.