to restraint stress (Ryan et al., 2012). Rosiglitazone also decreased circulating corticosterone levels in a mouse model of Alzheimer's disease (Escribano et al., 2009). While the mechanisms through which PPARs attenuate corticosterone remain to be fully elucidated, PPARα activation does interfere with GR-dependent gene expression by blocking the recruitment of RNA polymerase II to the glucocorticoid response elements on the promoter of GR target genes (Bougarne et al., 2009). While the effects of glucocorticoids after injury are complicated, it is apparent in these studies that PPARs play an integral role in this signaling pathway.
