Despite the traditionally limited clinical translational success associated with the focus on β-amyloid aggregation and tau protein hyperphosphorylation, recent evidence underscores the pivotal role of neuroinflammation, encompassing aberrant activation of microglia and astrocytes, disruption of the blood-brain barrier, and the involvement of systemic inflammatory mediators such as NLRP3 and CSF-1 in advancing AD pathology. Here, NLRP3 is linked to Alzheimer disease.