中国神经再生研究(英文版) ›› 2015, Vol. 10 ›› Issue (9): 1401-1402.doi: 10.4103/1673-5374.165507

• 观点:退行性病与再生 • 上一篇    下一篇

神经元基因转录可调节多发性硬化的小鼠模型的脱髓鞘和髓鞘再生 

  

  • 收稿日期:2015-08-18 出版日期:2015-09-28 发布日期:2015-09-28

Neuronal gene transcription modulates demyelination and remyelination in a mouse model of multiple sclerosis

Sofia Anastasiadou, Bernd Knöll   

  1. Institute of Physiological Chemistry, Ulm University, Ulm, Germany
  • Received:2015-08-18 Online:2015-09-28 Published:2015-09-28
  • Contact: Sofia Anastasiadou, sofia.anastasiadou@uni-ulm.de.

摘要:

多发性硬化是一种慢性炎症性脱髓鞘的中枢神经系统疾病。起病缓,易复发,后期可呈现进行性神经功能恶化。德国蒂宾根大学细胞生物学研究所Bernd Knöll教授最新研究表明,神经元和不同类型的神经胶质细胞的调节在病理性脱髓鞘和髓鞘再生过程可起着重要的作用。神经元积极参与大脑炎症细胞激活,从而调节髓鞘碎片清除。此外,Bernd Knöll教授强调,炎症在神经变性或神经保护中起着微妙平衡作用。多发性硬化当前的治疗策略旨在抑制中枢神经系统炎症和增强神经保护作用。因此,从啮齿类动物多发性硬化模型中得到分子和细胞机制的研究结果,可能有益于加深人类对多发性硬化发病机制的理解。例如在多发性硬化小鼠模型中SRF介导的基因转录的研究,能为人多发性硬化治疗提供有价值的新分子靶标。

Abstract:

Additionally, our data emphasize the delicate balance of inflammation leading either to neurodegeneration or neuroprotection. Current therapeutic strategies for MS aim at suppressing CNS inflammation and enhancing neuroprotection. Therefore, molecular and cellular insights obtained in rodent MS models, highlighting the importance of the neuronal compartment for disease progression, might prove useful for the understanding of mechanisms involved in the onset of human MS disease. Finally, the investigation of neuronal signaling mechanisms, such as SRF mediated gene transcription, identified in MS mouse models, might provide new valuable molecular targets relevant to human MS therapy.