Proinflammatory cytokines, indirectly, increase neurotoxic molecules by targeting indolamine-2,3-deoxigenaze (IDO) from tryptophan/kynurine metabolism pathways, which is majorly responsible for inflammation-induced (in vivo by lipopolysaccharide—LPS) deficit in memory and depression progress (Heisler and O’Connor, 2015). This evidence concerns the gene IDO1 and depressive symptom measurement.