Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia worldwide, characterized by progressive cognitive decline, memory impairment, and behavioral dysfunction. Despite extensive research, effective disease-modifying therapies remain limited, largely due to incomplete understanding of its complex and multifactorial pathogenesis. Increasing evidence now highlights chronic neuroinflammation as a central contributor to AD progression, shifting focus from a purely proteinopathy-based model toward an integrated neuroimmune perspective. Among key inflammatory pathways, the NLRP3 inflammasome has emerged as a critical innate immune signaling platform that links pathological protein aggregation to sustained neuroinflammatory responses in the central nervous system. Activation of the NLRP3 inflammasome is triggered by multiple Alzheimer’s disease–associated pathological stimuli, including amyloid-β accumulation, tau pathology, autophagy dysfunction, mitochondrial impairment, oxidative stress, and endoplasmic reticulum stress. These cellular disturbances converge to promote assembly of the inflammasome complex and activation of caspase-1. Activated caspase-1 mediates the proteolytic maturation and release of the pro-inflammatory cytokines interleukin-1β (IL-1β) and interleukin-18 (IL-18), both of which play central roles in amplifying neuroinflammatory signaling, promoting synaptic dysfunction, and contributing to neuronal injury. Consequently, IL-1β and IL-18 have gained increasing attention as potential biomarkers for disease severity, progression, and inflammatory burden in Alzheimer’s disease. In addition, inflammasome-specific markers such as apoptosis-associated speck-like protein containing CARD (ASC) specks provide further mechanistic and diagnostic evidence of active inflammasome signaling in neurodegeneration. Preclinical studies using cellular and animal models have demonstrated that pharmacological inhibition of the NLRP3 inflammasome can reduce neuroinflammation, attenuate neuropathological changes, and improve cognitive performance. However, despite these promising findings, clinical translation remains limited due to challenges including inadequate blood–brain barrier penetration, systemic immune modulation risks, and the absence of reliable biomarker-guided patient stratification strategies. This review critically examines the molecular mechanisms underlying NLRP3 inflammasome activation in Alzheimer’s disease, its interaction with pro-inflammatory cytokine networks, and the emerging role of inflammasome-related biomarkers in disease characterization. Furthermore, current therapeutic strategies targeting the NLRP3 pathway are discussed, along with key translational barriers and future directions for developing biomarker-driven immunomodulatory therapies in Alzheimer’s disease.