Role of NLRP3 Inflammasome in Alzheimer’s Disease

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder in elderly. Amyloid beta (Aβ) aggregation and its association with specific receptors on microglia initiate chronic inflammatory response. Nod like receptor family pyrin domain containing 3 gene (NLRP3) member of family of pattern recognition receptors (PRRs) initiate inflammation and apoptosis. NLPR3 inflammasome is a multiprotein complex and part of innate immune system. Injury induced activation of NLRP3 inflammasome via recognition of danger Associated molecular patterns (DAMPs) facilitate inflammasome complex formation and maturation of pro-IL-1β (and pro- IL-18) through caspases-1 and exacerbate the pathological condition by neuroinflammation. A review of the data shows that activation or inhibition of NLRP3 inflammasome leads to changes in process of neuroinflammation which may influence maturation and release of pro-IL-1β (and pro-IL-18) and Aβ accumulation and result in AD pathogenesis.