Remyelination as a therapeutic target in the treatment of multiple sclerosis

Multiple sclerosis (MS) is a chronic disease of the central nervous system (CNS) affecting young adults, particularly in North America and Europe, with nearly 2.5 million individuals impacted globally. Characterized by demyelination and neuronal damage, MS involves complex immune-mediated mechanisms. In this review, we focused on the pathophysiological processes of MS, highlighting the roles of T cells, B cells, and proinflammatory cytokines in driving demyelination, which are often the main focus of treatments in the form of immunotherapy. We emphasized remyelination as a key therapeutic target that is necessary for protecting axons and restoring neural function to solve the root problem. Emerging therapies, such as high-dose supplementation with vitamin D and glutathione, appear effective in regulating immune activity and lowering oxidative burden, thus supporting remyelination and neuroprotection. Preclinical models using toxin-induced demyelination have provided valuable insights into the mechanisms of remyelination and identified potential therapeutic targets like LINGO-1 antagonists. Clinical trials, particularly those involving the anti-LINGO-1 monoclonal antibody BIIB033, have demonstrated encouraging results in enhancing remyelination and improving clinical outcomes. LINGO-1 is an inhibitory protein that impairs OPC differentiation. Integrating these innovative approaches into clinical practice could revolutionize MS management by shifting the focus from managing symptoms to promoting CNS repair and long-term recovery. Continued research into the molecular mechanisms of remyelination and the development of targeted therapies is essential for advancing MS treatment and improving the quality of life for patients.