Neuroprotective Mechanisms of PPARδ: Modulation of Oxidative Stress and Inflammatory Processes. (29th October 2011)

• Record Type: Journal Article
• Authors: Schnegg, Caroline I.; Robbins, Mike E.
• Other Names: Drew Paul Academic Editor.
• Is Part Of: PPAR research. Volume 2011(2011)
• Publication Date: 2011-10-29
• Subjects: Peroxisomes -- Periodicals; Peroxisomal disorders -- Periodicals; 571.65505
• DOI: 10.1155/2011/373560
• Languages: English
• ISSNs: 1687-4757

Abstract

Abstract : Peroxisome proliferator-activated receptors (PPAR α, 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 PPAR α and PPAR γ are expressed in more restricted areas of the CNS, PPAR δ is ubiquitously expressed and is the predominant subtype. Although data regarding PPAR δ are limited, studies have demonstrated that administration of PPAR δ 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 PPAR δ agonists are thought to underly their neuroprotective efficacy. This review will focus on the putative neuroprotective benefits of therapeutically targeting PPAR δ in the CNS, and specifically, highlight the antioxidant and anti-inflammatory functions of PPAR δ agonists.