Multiple sclerosis (MS) is a T-cell-mediated autoimmune disease of the central nervous system (CNS). Worldwide, more than 2.3 million peo-ple are diagnosed with MS. Since its clinical manifestations appear typi-cally in the third and fourth decades of life, MS is a major cause of neu-rological disability in young adults and has wide health, psychological, economic, and social consequences. There are three key pathological features of MS: inflammation; demyelination and oligodendrocyte loss;axonal loss and neurodegeneration. There are two main hypotheses regarding mechanisms of MS pathology. The outside-in concept is an older, widely recognized hypothesis that describes neurodegeneration as a consequence of inflammatory induced demyelination, which is caused by immune system activation (Lassmann et al., 2012). Mecha-nisms of T-cell mediated myelin destruction are extensively studied, but the manner by which the immune system perceives myelin as foreign, and induces an autoimmune response is still unknown. The newer, in-side-out hypothesis considers MS to be a primary degenerative disor-der, which initiates in oligodendrocytes and results in neuroinflamma-tion that leads to demyelination (Stys et al., 2012). As one of the main pathological features of MS-pathology, induced neurodegenerative processes are present in different brain regions, including the hypothal-amus (Hyp).