Table of Contents Author Guidelines Submit a Manuscript
PPAR Research
Volume 2008, Article ID 538141, 7 pages
http://dx.doi.org/10.1155/2008/538141
Review Article

Peroxisome Proliferator-Activated Receptors: “Key” Regulators of Neuroinflammation after Traumatic Brain Injury

1Department of Orthopedic Surgery, Denver Health Medical Center, School of Medicine, University of Colorado, 777 Bannock Street, Denver, CO 80204, USA
2Division of Neurosurgery, Department of Surgery , Denver Health Medical Center, School of Medicine, University of Colorado, 777 Bannock Street, Denver, CO 80204, USA

Received 24 December 2007; Accepted 29 January 2008

Academic Editor: Paul Drew

Copyright © 2008 Philip F. Stahel 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.

Abstract

Traumatic brain injury is characterized by neuroinflammatory pathological sequelae which contribute to brain edema and delayed neuronal cell death. Until present, no specific pharmacological compound has been found, which attenuates these pathophysiological events and improves the outcome after head injury. Recent experimental studies suggest that targeting peroxisome proliferator-activated receptors (PPARs) may represent a new anti-inflammatory therapeutic concept for traumatic brain injury. PPARs are “key” transcription factors which inhibit NFκB activity and downstream transcription products, such as proinflammatory and proapoptotic cytokines. The present review outlines our current understanding of PPAR-mediated neuroprotective mechanisms in the injured brain and discusses potential future anti-inflammatory strategies for head-injured patients, with an emphasis on the putative beneficial combination therapy of synthetic cannabinoids (e.g., dexanabinol) with PPARα agonists (e.g., fenofibrate).