Mechanisms of remyelination: recent insight from experimental models

Biomolecular Concepts

Tanaka Tatsuhide¹  Yoshida Shigetaka¹ 

[1] Department of Functional Anatomy and Neuroscience, Asahikawa Medical University, Midorigaoka-higashi 2-1-1-1 Asahikawa, Hokkaido 078-8510, Japan;

关键词: cuprizone;    demyelination;    lysolecithin;    oligodendrocyte;    remyelination;   

DOI  :  10.1515/bmc-2014-0015

来源: DOAJ

【 摘 要 】

Oligodendrocytes and myelin play essential roles in the vertebrate central nervous system. Demyelination disrupts saltatory nerve conduction, leading to axonal degeneration and neurological disabilities. Remyelination is a regenerative process that replaces lost myelin. However, remyelination is disrupted in demyelinating diseases such as multiple sclerosis, at least partially, due to the failure of oligodendrocyte precursor cells to differentiate into myelinating oligodendrocytes. Understanding the molecular and cellular mechanisms that impact the differentiation of oligodendrocytes and myelination may help in the development of novel therapeutic strategies for demyelinating diseases. In this review, we focus on the molecular mechanisms controlling the differentiation of oligodendrocytes during remyelination, and we discuss the function of astrocytes and microglia in animal models of demyelinating diseases.

【 授权许可】

Unknown