Introduction

neurodegeneration, functional disability, immune-mediated disease, Chronic demyelinating lesions, mitochondrial dysfunction
NEURODEGENERATION, INFLAMMATION, MITOCHONDRIAL DYSFUNCTION, OXIDATIVE STRESS, DEMYELINATION, MULTIPLE SCLEROSIS (MS)
Multiple sclerosis (MS) is a chronic, immune-mediated disease of the central nervous system (CNS) that is characterized by inflammation, demyelination, and neurodegeneration [Remyelination of acutely denuded axons is one mechanism by which relapse recovery may occur. Remyelination may occur via newly differentiated oligodendrocytes, which are derived from oligodendrocyte precursor cells (OPCs) in the CNS. However, despite the presence of this innate repair mechanism, many patients later develop progressive functional disability. This may be due to a failure of remyelination or because of progressive axonal injury. Chronic demyelinating lesions are surrounded by OPCs and premyelinating oligodendrocytes, which suggest that failed remyelination does occur and could be partially due to incomplete oligodendrocyte differentiation [During development, thyroid hormones are essential for the development of the nervous system through enhancing neurogenesis, synaptogenesis, and glial cell differentiation promoting myelination. Hence, thyroid hormones may play a direct role in remyelination and repair in the adult CNS by promoting maturation of oligodendrocytes. Furthermore, thyroid hormones have been shown to reduce oxidative stress and thus may have the capacity to prevent mitochondrial dysfunction as well. In mice, tri-iodothyronine (T3) administration has been shown to help facilitate recovery from cuprizone-induced demyelination [