Abstract
Multiple sclerosis (MS) is a complex autoimmune disease of the central nervous system (CNS), which is characterized by demyelination and neurodegeneration. Oligodendrocytes have an essential role in maintaining the integrity of myelin, the protective sheath that surrounds nerve fibers and is indispensable for efficient signal transmission. Nevertheless, in multiple sclerosis, oligodendrocytes become dysfunctional, leading to myelin deterioration and axonal degeneration. Recent research suggests that metabolic changes, including mitochondrial dysfunction and alterations in glucose and lipid metabolism, contribute significantly to the pathogenesis of MS. Mitochondrial dysfunction is observed in both immune cells and CNS oligodendrocytes of MS patients. Impaired mitochondrial function leads to energy deficits, affecting crucial processes such as impulse transmission and axonal transport, ultimately contributing to neurodegeneration. Understanding the complex relationship between these mechanisms is crucial to the development of an effective treatment for MS.
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