Therefore, we speculate that exogenous supplementation of tryptophan derivatives (such as FICZ, IAId), or targeted intervention of GM (such as Lactobacillus reuteri, Lactobacillus salivary, Bifidobacterium and Lactobacillus), or targeted induction of the Kyn-IDO pathway to accelerate endogenous tryptophan metabolism and produce AhR ligands, may ultimately alleviate clinical symptoms of AD by suppressing abnormal immune responses. The gene discussed is IDO1; the disease is Alzheimer disease.