It is shown that fibrillar amyloid β (Aβ) can directly interact with Toll-like receptor 2 (TLR2), TLR4, and CD14 to induce microglial Aβ phagocytosis at the initial stages and neuroinflammatory responses at the late stages of Alzheimer's disease [112]. The gene discussed is TLR4; the disease is early-onset autosomal dominant Alzheimer disease.