Multiple sclerosis (MS) is a chronic, multifactorial autoimmune disease of the central nervous system (CNS), characterized by inflammation, demyelination, and neurodegeneration. The etiology of MS remains unknown, but both genetic predisposition and environmental factors contribute to disease susceptibility. The pathophysiology involves autoreactive T- and B-cells that induce myelin damage, leading to progressive neurological decline. Recent research highlights metabolic alterations in MS, including changes in glucose metabolism, mitochondrial dysfunction, and oxidative stress, contributing to neuroinflammation and disease progression. Current therapies primarily modulate immune responses to reduce relapses and slow progression, but neuroprotective and remyelinating treatments remain an unmet need. Advances in metabolic profiling and immunometabolic interventions may offer novel therapeutic avenues in the future.