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中，髓鞘再生（髓鞘再生）是设计神经保护疗法的关键研究策略。然而，与没有脊髓病变的患者相比，脊髓MS病变的患者具有重要的残疾（行走减少和膀胱衰竭）和更差的长期结局。病理学数据表明，脊髓中的髓鞘再生比大脑中的效率低。然而，为什么脊髓中髓鞘再生较差尚不清楚，这阻碍了对患者进行最佳分层以获得最合适的治疗方法。该项目将解决这个问题，使用人类和斑马鱼的转录组数据集，生成假设，然后将在斑马鱼作为体内模型生物和人类死后组织中进行测试。

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.