Our working model proposes that in the homeostatic state, tryptophan catabolism keeps KYNA/Ahr2 and serotonin/Htr1 signaling active, while amyloid-induced neuropathology suppresses the tryptophan metabolism through Interleukin-4, which leads to potentiation of BDNF/Ngfra signaling in NSCs and induces direct regulation of NSC plasticity through IL4/Il4r signal transduction [1,2,3,4,9,10,11,12,51] (Figure 6B). Here, IL4 is linked to amyloidosis.