کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
1905260 1534699 2011 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Cells of the oligodendroglial lineage, myelination, and remyelination
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی سالمندی
پیش نمایش صفحه اول مقاله
Cells of the oligodendroglial lineage, myelination, and remyelination
چکیده انگلیسی

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.

Research Highlights
► The oligodendrocyte is the CNS cell type responsible for production of the myelin sheath.
► Newly differentiated oligodendrocyte progenitor cells mediate myelin repair (remyelination).
► Transplantation of exogenous progenitors or targeting endogenous ones may enhance remyelination.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1812, Issue 2, February 2011, Pages 184–193
نویسندگان
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