While previous studies using candidate approaches show that dysregulated levels of several specific cytokines including IL-33, NLRP3 inflammasome, IL-12/IL-23, and IL-10 are associated with AD pathogenesis [15, 26–30], modulating these cytokine signaling pathways in mouse models of amyloidosis and hyperphosphorylated tau results in beneficial outcomes. This evidence concerns the gene IL23A and amyloidosis.