In addition, we found that inhibition of IDO activation ameliorated the activity deficits of mitochondrial respiratory chain complexes I and IV, a finding that echoes previous studies: mitochondrial abnormalities is directly involved in excitotoxicity-induced neuronal death and is strongly associated with epilepsy-related cognitive deficits [62,63] whereas targeted antioxidant interventions (e.g., hydrogen therapy) can indirectly inhibit epileptic networks by attenuating hippocampal oxidative damage [64]. This evidence concerns the gene NDUFV1 and Cognitive impairment.