In Down syndrome, increased tryptophan oxidation as a function of interferon-induced indole 2,3-dioxygenase (IDO1) activity results in the accumulation of neurotoxic metabolites like kynurenine and picolinic acid [66], potential contributors to the neurocognitive decline observed in the Down syndrome population [30,35] and, in general, during aging. This evidence concerns the gene IDO1 and Down syndrome.