Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA.
Department of Neuroscience, Georgetown University Medical Center, Georgetown University, Washington, District of Columbia, USA.
J Clin Invest. 2019 Oct 1;129(10):4365-4376. doi: 10.1172/JCI126809.
Inflammatory destruction of iron-rich myelin is characteristic of multiple sclerosis (MS). Although iron is needed for oligodendrocytes to produce myelin during development, its deposition has also been linked to neurodegeneration and inflammation, including in MS. We report perivascular iron deposition in multiple sclerosis lesions that was mirrored in 72 lesions from 13 marmosets with experimental autoimmune encephalomyelitis. Iron accumulated mainly inside microglia/macrophages from 6 weeks after demyelination. Consistently, expression of transferrin receptor, the brain's main iron-influx protein, increased as lesions aged. Iron was uncorrelated with inflammation and postdated initial demyelination, suggesting that iron is not directly pathogenic. Iron homeostasis was at least partially restored in remyelinated, but not persistently demyelinated, lesions. Taken together, our results suggest that iron accumulation in the weeks after inflammatory demyelination may contribute to lesion repair rather than inflammatory demyelination per se.
富含铁的髓磷脂的炎症性破坏是多发性硬化症 (MS) 的特征。尽管铁对于少突胶质细胞在发育过程中产生髓磷脂是必需的,但铁的沉积也与神经退行性变和炎症有关,包括在 MS 中。我们报告了多发性硬化症病变中的血管周围铁沉积,这在 13 只患有实验性自身免疫性脑脊髓炎的狨猴的 72 个病变中得到了反映。铁主要在脱髓鞘后 6 周内积累在小胶质细胞/巨噬细胞内。一致的是,转铁蛋白受体(大脑的主要铁内流蛋白)的表达随着病变的老化而增加。铁与炎症无关,也与最初的脱髓鞘无关,这表明铁不是直接致病的。在再髓鞘化但不持续脱髓鞘的病变中,铁稳态至少部分得到了恢复。总之,我们的结果表明,在炎症性脱髓鞘后的数周内铁的积累可能有助于病变修复,而不是炎症性脱髓鞘本身。