There are two published microarray analyses of brain gene expression after PPAR agonist treatment. First, Chikahisa and colleagues fed mice a beza diet and analyzed brain gene expression in the hypothalamus to assess the effects of PPAR activation on circadian rhythm 11. Several genes were commonly regulated by beza in their dataset and in our amygdala and PFC datasets, including Arpp21, Chmp4b, Crem, Psmc3ip and Dtnb. Second, Searcy and colleagues delivered pioglitazone, a PPARγ agonist, to triple transgenic Tg mice (a line used to model Alzheimer’s disease) and analyzed its effect on brain gene expression in the hippocampus 56. Despite many experimental differences between this study and ours, there are remarkable similarities in the gene expression profiles. The overlap between their top-table and ours was greater than expected by chance for all PPAR agonist treatments in the amygdala, especially tesa (p=9.5e-08), and for tesa treatment in the PFC (p=3.09e-05). This is consistent with the activity of tesa at PPARγ (Table S6). ORA of the Searcy dataset did not support an overall pioglitazone-mediated suppression of inflammatory processes, which is consistent with
