Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder predominantly affecting the elderly, characterized by memory loss, cognitive decline, and functional impairment. While hallmark pathological features include extracellular amyloid beta (Aβ) plaques and intracellular neurofibrillary tangles composed of hyperphosphorylated tau protein, increasing evidence points to chronic neuroinflammation as a key driver of disease progression. Among inflammatory mechanisms, the activation of the NLRP3 (nucleotide-binding domain, leucine-rich repeat, and pyrin domain-containing protein 3) inflammasome in microglia plays a pivotal role by amplifying neuroinflammatory cascades, exacerbating synaptic dysfunction, and accelerating neuronal loss. This review examines the molecular underpinnings of AD with a focus on NLRP3 inflammasome-mediated neuroinflammation, detailing the crosstalk between Aβ, tau pathology, and innate immune responses. Finally, we highlight emerging therapeutic strategies targeting NLRP3 inflammasome activation as promising avenues for mitigating neuroinflammation and slowing AD progression.