The role of glial-neuronal metabolic cooperation in modulating progression of multiple sclerosis and neuropathic pain
The role of glial-neuronal metabolic cooperation in modulating progression of multiple sclerosis and neuropathic pain
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DOI：
10.2217/imt-2018-0153
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发表时间：
2019-02-01
期刊：
影响因子：
2.8
通讯作者：
Forsthuber, Thomas G.
中科院分区：
文献类型：
--
作者：
Robinson, Rachel R.;Dietz, Alina K.;Forsthuber, Thomas G.
虽然多发性硬化症 (MS) 的病因尚不清楚，但临床和临床前模型的研究确定了炎症和脱髓鞘在 MS 发病机制中的重要作用。目前专注于抗炎过程的治疗对于急性发作和复发缓解型多发性硬化症有效，但患者仍会发展为继发进展性多发性硬化症。 MS 的进展与小胶质细胞和星形胶质细胞的激活有关，更重要的是，代谢功能障碍导致神经元死亡。神经元死亡也会导致慢性神经性疼痛。神经胶质细胞对神经元的代谢支持可能在预防多发性硬化症和慢性神经性疼痛的进展中发挥核心作用。在这里，我们回顾了神经胶质细胞和神经元之间的代谢合作机制，并概述了探索神经胶质细胞对神经元代谢支持的未来前景。
While the etiology of multiple sclerosis (MS) remains unclear, research from the clinic and preclinical models identified the essential role of inflammation and demyelination in the pathogenesis of MS. Current treatments focused on anti-inflammatory processes are effective against acute episodes and relapsing-remitting MS, but patients still move on to develop secondary progressive MS. MS progression is associated with activation of microglia and astrocytes, and importantly, metabolic dysfunction leading to neuronal death. Neuronal death also contributes to chronic neuropathic pain. Metabolic support of neurons by glia may play central roles in preventing progression of MS and chronic neuropathic pain. Here, we review mechanisms of metabolic cooperation between glia and neurons and outline future perspectives exploring metabolic support of neurons by glia.