الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Multiple Sclerosis (MS) is a debilitating disease of the central nervous system (CNS) and its pathological hallmarks are plaques of demyelination in the CNS, with surrounding area of inflammation and neurodegeneration. It is characterized by the predominant presentation in young women compared to men.
Loss of myelin sheath in demyelinating disorders leads to loss of salutatory conduction, physical protection and metabolic support and causes neurodegeneration.
In multiple sclerosis, partly remyelinated lesions characterized by their intermediate levels of myelin, can be observed as a neuropathological criterion for repair activity, this remyelination is affected by variety of factors such as sex, genetic background, age, the presence of multiple differentiation inhibitors that specifically restrict the glial regeneration potential.
Remyelination-related steps such as oligodendrocyte progenitor cells (OPC) activation, recruitment, differentiation, and myelination are tightly regulated by a number of extrinsic and intrinsic factors that act either as inhibitors or activators of remyelination such as Notch-1, LINGO-1, Went/ ß-catenin pathway, retinoid X receptor gamma (RXR- γ) pathway. Targeting these pathways may provide a potential putative remyelination therapy.
The present study is designed to assess the possible role of quercetin, pioglitazone, metforminand dapagliflozin in enhancement of remyelination after induction of demyelination.