The Impact of Iron Metabolism in the Pathogenesis of Multiple Sclerosis

Abstract

Objective: Multiple sclerosis (MS) is a chronic disease of the central nervous system (CNS) leading to oligodendrocyte destruction, demyelination, remyelination, astrocytic scar formation, and neurodegeneration, all being associated with inflammation. Iron may contribute to the pathogenesis and progression of MS due to its accumulation in the human brain with age. It is unclear whether iron metabolism plays a role in the pathogenesis of MS. In this study, our aim was to investigate the possible role of dysfunctional iron metabolism in the pathogenesis of MS. Material and Methods: The study consisted of 32 patients with MS, and 30 age-matched healthy controls. Seven patients had relapsing remitting active (RRMS-A), 7 had relapsing-remitting stable (RRMSS), 10 had secondary progressive disease (SPMS) and 8 had progressive relapsing (PRMS) disease. We analyzed hemoglobin, iron, transferrin and soluble transferrin receptor (sTfR) levels in MS patients and compared with controls. Results: There was no significant difference in terms of age between patients with MS (mean age, 36.85±7.23 years, n=32) and control group (mean age, 34.26±6.85 years; n=30). The sTfR levels were significantly higher in MS patients compared to the control group (p<0.05). Conclusion: The increased serum sTfR levels in MS patients may reflect an increased iron turnover, due to inflammatory and oxidative stres. Iron chelating therapies for MS patients can therefore, based on our current knowledge, not be recommended. Nevertheless, blocking harmful downstream effects of iron liberation, such as oxidation of lipids and DNA, might be beneficial for MS patients.