There are several underlying mechanisms that may account for the association of IDO1 with PSD: the elevated levels of pro-inflammatory cytokines after stroke upregulate IDO1 expression that causes the depletion of serotonin precursor tryptophan and increased neurotoxic kynurenine metabolite (quinolinic acid), an agonist of NMDA receptors, leading to the occurrence of depression (14, 30–32). This evidence concerns the gene IDO1 and depressive symptom measurement.