The underlying cause of MS is considered to be a combination of genetic susceptibility, lifestyle, and environmental factors. Although early-stage MS patients usually experience a partial recovery after each attack, a consistent progressive course will eventually take over, featuring central nervous system (CNS) degeneration and gradually aggravated disability, posing challenges for effective treatment. Multiple sclerosis (MS), the chronic demyelinating neuroautoimmune disease, is a prevalent cause of disability among the youth, unfortunately still uncurable. The remaining area of ambiguity requires further exploration into this arena to validate the existed phenomenon, develop novel therapies, and confirm the safety and efficacy of therapeutic intervention targeting FA metabolism. In addition, FAs are indeed protective factors for blood–brain barrier integrity, crucial contributors of central nervous system (CNS) chronic inflammation and progressive degeneration, as well as important materials for remyelination. FA and FA metabolism are highly associated with autoimmunity, as the diet-derived circulatory and tissue-resident FAs level and composition can modulate immune cells polarization, differentiation and function, suggesting their broad regulatory role as “metabokines”. Fatty acids (FA) and MS bear an interesting intimate connection. Multiple sclerosis (MS), as an autoimmune neurological disease with both genetic and environmental contribution, still lacks effective treatment options among progressive patients, highlighting the need to re-evaluate disease innate properties in search for novel therapeutic targets.
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