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PPAR Research
Volume 2011, Article ID 373560, 10 pages
http://dx.doi.org/10.1155/2011/373560
Review Article

Neuroprotective Mechanisms of PPARδ: Modulation of Oxidative Stress and Inflammatory Processes

1Department of Cancer Biology, Comprehensive Cancer Center, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA
2Brain Tumor Center of Excellence, Comprehensive Cancer Center, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA
3Department of Radiation Oncology, Comprehensive Cancer Center, Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA

Received 28 July 2011; Accepted 25 August 2011

Academic Editor: Paul Drew

Copyright © 2011 Caroline I. Schnegg and Mike E. Robbins. 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

Peroxisome proliferator-activated receptors (PPARα, δ, and γ) are ligand-activated transcription factors that regulate a wide range of cellular processes, including inflammation, proliferation, differentiation, metabolism, and energy homeostasis. All three PPAR subtypes have been identified in the central nervous system (CNS) of rodents. While PPARα and PPARγ are expressed in more restricted areas of the CNS, PPARδ is ubiquitously expressed and is the predominant subtype. Although data regarding PPARδ are limited, studies have demonstrated that administration of PPARδ agonists confers neuroprotection following various acute and chronic injuries to the CNS, such as stroke, multiple sclerosis, and Alzheimer's disease. The antioxidant and anti-inflammatory properties of PPARδ agonists are thought to underly their neuroprotective efficacy. This review will focus on the putative neuroprotective benefits of therapeutically targeting PPARδ in the CNS, and specifically, highlight the antioxidant and anti-inflammatory functions of PPARδ agonists.