再髓鞘化
星形胶质细胞
多发性硬化
髓鞘
背景(考古学)
少突胶质细胞
神经科学
生物
炎症
胶质瘢痕
病理
免疫学
医学
中枢神经系统
古生物学
作者
Markus Kipp,Tim Clarner,Stefan Gingele,Friederike Pott,Sandra Amor,Paul van der Valk,Cordian Beyer
出处
期刊:Physiological Research
[Institute of Physiology of the Czech Academy of Sciences]
日期:2011-10-15
卷期号:: S49-S60
被引量:37
标识
DOI:10.33549/physiolres.932168
摘要
Over a century ago, hyperplasia and hypertrophy of astrocytes was noted as a histopathological hallmark of multiple sclerosis and was hypothesized to play an important role in the development and course of this disease. However until today, the factual contribution of astrocytes to multiple sclerosis is elusive. Astrocytes may play an active role during degeneration and demyelination by controlling local inflammation in the CNS, provoking damage of oligodendrocytes and axons, and glial scarring but might also be beneficial by creating a permissive environment for remyelination and oligodendrocyte precursor migration, proliferation, and differentiation. Recent findings from our lab suggest that brain lipid binding protein (FABP7) is implicated in the course of multiple sclerosis and the regulation of astrocyte function. The relevance of our findings and data from other groups are highlighted and discussed in this paper in the context of myelin repair.
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