<p>Alzheimer’s disease is a progressive neurodegenerative disorder characterized by early synaptic dysfunction that precedes overt neuronal loss and cognitive decline. While amyloid-β and tau pathologies have long dominated disease models, growing evidence highlights neuroinflammation as a critical driver of early pathological changes. In particular, microglia-mediated inflammatory signaling has emerged as a key regulator of synaptic integrity. This review focuses on the interleukin-1β (IL-1β)-NLRP3 inflammasome axis as a central mechanism linking innate immune activation to aberrant synaptic pruning in early Alzheimer’s disease. Activation of the NLRP3 inflammasome in microglia by amyloid-β and related danger signals leads to caspase-1-dependent maturation and release of IL-1β. Elevated IL-1β amplifies inflammatory signaling, alters microglial phenotype, and promotes complement-mediated tagging of synapses, resulting in excessive elimination of functional synaptic connections. Experimental evidence from in vitro systems, transgenic mouse models, and pharmacological inhibition studies supports a causal role for this axis in synapse loss, impaired synaptic plasticity, and cognitive deficits. Importantly, these inflammatory and synaptic alterations occur at early disease stages, underscoring their relevance to disease initiation rather than late-stage neurodegeneration. The review further discusses the impact of IL-1β-NLRP3 signaling on neuronal network function, hippocampal plasticity, and cognitive performance, as well as its translational implications. Therapeutic strategies targeting inflammasome activation or IL-1β signaling show promise in preserving synaptic function in preclinical models. Overall, the IL-1β-NLRP3-synapse axis represents a compelling framework for understanding early Alzheimer’s disease pathology and offers a rational target for early intervention strategies to slow disease progression.</p>