期刊
NEURAL REGENERATION RESEARCH
卷 16, 期 7, 页码 1359-1368出版社
WOLTERS KLUWER MEDKNOW PUBLICATIONS
DOI: 10.4103/1673-5374.300975
关键词
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资金
- National Institute of Neurological Disorders and Stroke of the National Institutes of Health [R21 NS098170]
- Kentucky Spinal Cord and Head Injury Research Trust [16-3A]
- National Natural Science Foundation of China [81601957]
Multiple sclerosis is an autoimmune disease that affects the central nervous system by attacking the myelin sheath. Glial cells play a crucial role in neuroinflammation and neurodegeneration associated with multiple sclerosis. Maintaining a balanced glial response is important for efficient remyelination and neuroregeneration.
Multiple sclerosis is an autoimmune disease in which the immune system attacks the myelin sheath in the central nervous system. It is characterized by blood-brain barrier dysfunction throughout the course of multiple sclerosis, followed by the entry of immune cells and activation of local microglia and astrocytes. Glial cells (microglia, astrocytes, and oligodendrocyte lineage cells) are known as the important mediators of neuroinflammation, all of which play major roles in the pathogenesis of multiple sclerosis. Network communications between glial cells affect the activities of oligodendrocyte lineage cells and influence the demyelination-remyelination process. A finely balanced glial response may create a favorable lesion environment for efficient remyelination and neuroregeneration. This review focuses on glial response and neurodegeneration based on the findings from multiple sclerosis and major rodent demyelination models. In particular, glial interaction and molecular crosstalk are discussed to provide insights into the potential cell- and molecule-specific therapeutic targets to improve remyelination and neuroregeneration.
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