神经炎症
再髓鞘化
多发性硬化
少突胶质细胞
神经科学
小胶质细胞
生物
中枢神经系统
炎症
免疫系统
白质
创伤性脑损伤
脱髓鞘病
免疫学
髓鞘
医学
放射科
精神科
磁共振成像
作者
Lindsay Festa,Kelly L. Jordan‐Sciutto,Judith B. Grinspan
出处
期刊:Glia
[Wiley]
日期:2025-03-10
摘要
Chronic neuroinflammation, driven by central nervous system (CNS)-resident astrocytes and microglia, as well as infiltration of the peripheral immune system, is an important pathologic mechanism across a range of neurologic diseases. For decades, research focused almost exclusively on how neuroinflammation impacted neuronal function; however, there is accumulating evidence that injury to the oligodendrocyte lineage is an important component for both pathologic and clinical outcomes. While oligodendrocytes are able to undergo an endogenous repair process known as remyelination, this process becomes inefficient and usually fails in the presence of sustained inflammation. The present review focuses on our current knowledge regarding activation of the innate and adaptive immune systems in the chronic demyelinating disease, multiple sclerosis, and provides evidence that sustained neuroinflammation in other neurologic conditions, such as perinatal white matter injury, traumatic brain injury, and viral infections, converges on oligodendrocyte injury. Lastly, the therapeutic potential of targeting the impact of inflammation on the oligodendrocyte lineage in these diseases is discussed.
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