For instance, in Alzheimer‘s disease (AD), fibrillar amyloid-β (Aβ) deposits engage microglial pattern recognition receptors (e.g., TLR4), leading to NLRP3 inflammasome activation, which exacerbates tau hyperphosphorylation and cognitive deficits in murine models [10,11]. The gene discussed is MAPT; the disease is Alzheimer disease.