Multiple sclerosis (MS), characterized by inflammatory demyelination in the central nervous system, is a complex autoimmune disorder. Prominent symptoms include damage to myelin sheaths in the brain, optic nerve, and spinal cord, as well as axonal dysfunction. The exact causes and mechanisms of MS remain unclear. It is believed that genetic and environmental factors interact through 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, the author reviewed relevant literature from the past decade, summarizing the mechanisms underlying NLRP3 activation and its connection to MS. Based on a comprehensive review of literature published over the past decade, this article systematically analyzes the molecular mechanisms and activation pathways of the NLRP3 inflammasome, as well as its pathological interplay with MS. The findings aim to provide insights into disease progression and potential therapeutic strategies by elucidating the underlying mechanisms involved.