Why don't spinal cord OPCs remyelinate well in multiple sclerosis and how do we fix it?

在多发性硬化症(MS)中，髓鞘损伤发生在大脑和脊髓，髓鞘再生(重新髓鞘形成)是设计神经保护疗法的关键研究策略。然而，有脊髓多发性硬化症病变的患者与无脊髓病变的患者相比，有重要的残疾(行走和膀胱衰竭减少)和较差的长期结果。病理数据表明，脊髓中的再髓鞘形成不如大脑中的有效。然而，为什么脊髓中的再髓鞘形成较差尚不清楚，这阻碍了患者获得最合适的治疗方法的最佳分层。这个项目将解决这个问题，使用来自人类和斑马鱼的转录数据集，产生假说，然后在斑马鱼身上作为活体模型生物和人类死后组织进行测试。

In multiple sclerosis (MS), myelin damage occurs in the brain and spinal cord, and regeneration of myelin (remyelination) is a key research strategy to design therapies for neuroprotection. However, patients with spinal cord MS lesions have important disability (reduced walking and bladder failure) and poorer long-term outcomes than without spinal cord lesions. Pathological data suggest that remyelination in the spinal cord is less efficient than in the brain. However, why remyelination is poorer in the spinal cord is not clear, hampering best stratification of patients for the most appropriate therapeutics. This project will tackle this question, using transcriptomic datasets from human and zebrafish, generating hypotheses that will then be tested in zebrafish as an in vivo model organism and on human post mortem tissue.