Multiple sclerosis (MS) is a complex autoimmune disorder characterized by inflammatory demyelination in the central nervous system. Prominent symptoms include damage to myelin sheaths in the brain, optic nerve, and spinal cord, as well as axonal dysfunction; however, the exact causes and mechanisms of MS remain unclear. Genetic and environmental factors are thought to interact via autoimmune mechanisms, potentially triggering the disease. Recent studies suggest that abnormal activation of the NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome may play a critical role in the pathogenesis of MS. In this context, this review summarizes the molecular mechanisms underlying NLRP3 activation and its connection to MS, considering relevant literature from the past decade. The findings aim to provide insights into the progression of MS and to identify potential therapeutic strategies by elucidating the underlying mechanisms.