Figure 2: Clues and possible interactions between amyloid β, tau pathology, and innate immunity. Amyloid β is capable of activating complement system and microglia, inducing release of many cytokines and activating NLRP3 inflammasome. Soluble amyloid β oligomers may bind to TLR4, TLR6, and CD36 on microglial cell surface and cause their activation. Microglia release pro-inflammatory cytokines. These cytokines are also capable of inducing amyloid protein expression and CDK 5 activity, thus further increasing amyloid and tau pathology. NLRP3 inflammasome increases tau phosphorylation and aggregation. Notice all the elements being part of innate immunity