中国神经再生研究(英文版) ›› 2019, Vol. 14 ›› Issue (10): 1715-1716.doi: 10.4103/1673-5374.257525

• 观点:退行性病与再生 • 上一篇    下一篇

新型体外脱髓鞘/髓鞘再生模型可复制多发性硬化症和视神经脊髓炎

  

  • 出版日期:2019-10-15 发布日期:2019-10-15

New ex vivo demyelination/remyelination models to defeat multiple sclerosis and neuromyelitis optica

Yiting Liu   

  1. De Department of Neurology, School of Medicine, University of Colorado, Aurora, CO, USA
  • Online:2019-10-15 Published:2019-10-15
  • Contact: Yiting Liu, PhD, Yiting.liu@ucdenver.edu
  • Supported by:

    This work was supported by National Multiple Sclerosis Society, NIH and the Guthy-Jackson Charitable Foundation.

摘要:

orcid:0000-0002-0083-1803 (Yiting Liu)

Abstract:

Multiple sclerosis (MS) and neuromyelitis optica (NMO) are inflammatory diseases of the central nervous system (CNS) resulting in CNS inflammation, infiltration of peripheral immune cells, loss of myelin and oligodendrocytes, interruption of axonal communication, and neurologic deficits. Following oligodendrocyte injury, newly generated myelinating oligodendrocytes derived from oligodendrocyte progenitors (OPCs) may produce new myelin sheaths around denuded axons (remyelination) restoring neuronal function. While remyelination is apparent in MS lesions, the process is often inefficient; in NMO, remyelination is even more limited. Currently, there are no restorative therapies for MS and NMO. Understanding the mechanisms underlying driving disease-specific myelin damage and repair is critical to identify remyelination barriers and develop new treatments promoting remyelination. Current studies to understand the molecular and cellular events regulating demyelination and remyelination processes have employed developmental, toxic, and caustic models of oligodendrocyte injury. These models cannot replicate the inflammatory pathology of demyelination in MS and NMO, and fail to replicate the milieu that may inhibit repair.