Abstract: Multiple sclerosis (MS) is a T-cell-mediated autoimmune disease of the central nervous system (CNS). Worldwide, more than 2.3 million people are diagnosed with MS. Since its clinical manifestations appear typically in the third and fourth decades of life, MS is a major cause of neurological 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). Mechanisms 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, “inside- out” hypothesis considers MS to be a primary degenerative disorder, which initiates in oligodendrocytes and results in neuroinflammation 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 hypothalamus (Hyp).