It inhibited NLRP3 inflammasome activation by reducing NLRP3, apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC), cleaved caspase-1, IL-1β, and IL-18 levels, and thus, boosted the brain-derived neurotrophic factor/tropomyosin receptor kinase B (TrkB) signaling pathway, as a result of which cognitive impairment was attenuated in streptozotocin-induced diabetic rats [127]. Here, NLRP3 is linked to Cognitive impairment.