Cerebral iron accumulation in multiple sclerosis: Pathophysiology and therapeutic implications

Multiple sclerosis (MS) is a chronic autoimmune disorder of the central nervous system characterized by demyelination, neuroinflammation, and neurodegeneration. Recent studies highlight the role of cerebral iron (Fe) accumulation in exacerbating MS pathophysiology. Fe, essential for neural function, contributes to oxidative stress and inflammation when dysregulated, particularly in the brain's gray matter and demyelinated lesions. Advanced imaging techniques, including susceptibility-weighted and quantitative susceptibility mapping, have revealed abnormal Fe deposition patterns in MS patients, suggesting its involvement in disease progression. Iron's interaction with immune cells, such as microglia, releases pro-inflammatory cytokines, further amplifying neuroinflammation and neuronal damage. These findings implicate Fe dysregulation as a significant factor in MS progression, contributing to clinical manifestations like cognitive impairment. Therapeutic strategies targeting Fe metabolism, including Fe chelation therapies, show promise in reducing Fe-related damage, instilling optimism about the future of MS treatment. However, challenges such as crossing the blood-brain barrier and maintaining Fe homeostasis remain. Emerging approaches, such as Fe-targeted nanotherapeutics and biologics, offer new possibilities for personalized treatments. However, the journey is far from over. Continued research into the molecular mechanisms of Fe-induced neuroinflammation and oxidative damage is essential. Through this research, we can develop effective interventions that could slow MS progression and improve patient outcomes.