Abstract
In a recent issue of Experimental Neurology, Sauerbeck and colleagues demonstrated that treatment with the peroxisome proliferator-activated receptor (PPAR) agonist Pioglitazone after experimental traumatic brain injury (TBI) in rats was protective against mitochondrial dysfunction, cognitive impairment, cortical tissue loss and microglial activation. In this commentary, we review the key findings of this work and their relevance to previous and future neurotrauma research. More broadly, we speculate about their significance in the context of developing therapeutic strategies for a wide range of neuroinflammatory conditions.