Cells of the oligodendroglial lineage, myelination, and remyelination

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE

卷:1812

Review

Miron, Veronique E.²  Kuhlmann, Tanja³  Antel, Jack P.¹ 

[1] McGill Univ, Montreal Neurol Inst, Neuroimmunol Unit, Montreal, PQ H3A 2B4, Canada

[2] Univ Edinburgh, Queens Med Res Inst, Ctr Regenerat Med, Edinburgh EH16 4TJ, Midlothian, Scotland

[3] Univ Hosp, Inst Neuropathol, D-37075 Gottingen, Germany

关键词: Myelin;    Remyelination;    Oligodendrocyte;    Oligodendrocyte progenitor cell;    Multiple sclerosis;    Repair;   

DOI  :  10.1016/j.bbadis.2010.09.010

来源: Elsevier

【 摘 要 】

Myelin is critical in maintaining electrical impulse conduction in the central nervous system. The oligodendrocyte is the cell type responsible for myelin production within this compartment. The mutual supply of trophic support between oligodendrocytes and the underlying axons may indicate why demyelinated axons undergo degeneration more readily; the latter contributes to the neural decline in multiple sclerosis (MS). Myelin repair, termed remyelination, occurs in acute inflammatory lesions in MS and is associated with functional recovery and clinical remittances. Animal models have demonstrated that remyelination is mediated by oligodendrocyte progenitor cells (OPCs) which have responded to chemotactic cues, migrated into the lesion, proliferated, differentiated into mature oligodendrocytes, and ensheathed demyelinated axons. The limited remyelination observed in more chronic MS lesions may reflect intrinsic properties of neural cells or extrinsic deterrents. Therapeutic strategies currently under development include transplantation of exogenous OPCs and promotion of remyelination by endogenous OPCs. All currently approved MS therapies are aimed at dampening the immune response and are not directly targeting neural processes. (C) 2010 Elsevier B.V. All rights reserved.

【 授权许可】

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