الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Myelin sheath, a discontinuous fatty insulation that ensheaths axons, is critical for the normal function of nervous system. Loss of myelin sheath in demyelinating disorders leads to loss of saltatory conduction, physical protection and metabolic support and causes neurodegeneration. Up till now, there are no disease-modifying drugs to efficiently slow, stop or reverse neurodegeneration in demyelinating diseases.
Neuroprotective drugs have been proposed for other neurological diseases, including stroke, spinal cord injury and Alzheimer’s disease, with limited success. However, an alternative strategy is available in demyelinating disorders, where neuroprotection may be enhanced through two ways either to use drugs that directly protect axons, or drugs that improve remyelination, which restores the support of axons. It was found that population of oligodendrocyte precursor cells (OPCs) is likely responsible for generating almost all remyelinating cells in demyelinating lesions in the adult CNS. Preexisting mature oligodendrocytes are unlikely to contribute to remyelination.
As, multiple sclerosis (MS) is the most common autoimmune disorder affecting the central nervous system and its pathological hallmarks are plaques of demyelination in the CNS, with surrounding area of inflammation and neurodegeneration, animal model of multiple sclerosis is selected in this work to study the possible effect of enhancing remyelination in improvement of pathological events associated with demyelination.