Several studies have employed mitochondria-targeted drugs in TBI models to increase mitochondrial biogenesis with the aim to reduce brain damage after injury [59] but here we saw downregulation of such genes namely, mRpL55 and mRpL43. The absence of upregulation of immune system and mitochondrial genes could indicate that Tau deficiency is neuroprotective in brain injury. This evidence concerns the gene MAPT and hyperinsulinemic hypoglycemia, familial, 4.