Therefore, the upregulation of PPARɣ induced by mTBI might be a mechanism to promote insulin sensitivity and enhance glucose metabolism; on the other hand, the downregulation of PPARɑ might outline a reduced triglyceride metabolism with a subsequent overall dysregulation in energy homeostasis that might contribute to the development of AD induced by brain trauma in genetically predisposed mice. The gene discussed is PPARA; the disease is Alzheimer disease.