SYNAPTIC CHANGES AND ASSOCIATED ASTROCYTE MECHANISMS IN A MODEL OF MULTIPLE SCLEROSIS AND AFTER TREATMENT WITH FINGOLIMOD

Multiple sclerosis (MS) is a demyelinating and inflammatory disease of the Central Nervous System (CNS), which causes various cognitive, motor and sensory impairments, including the visual ones. In addition to the classic inflammatory cascade and demyelinating lesions, synaptopathy has recently been added to the pathophysiological mechanisms of MS, and it can arise even before the loss of myelin. Astrocytes are one of the key regulators of synaptic formation and function through soluble factor secretion and contact-dependent mechanisms. In MS lesion sites, they correspond to one of the primary and striking elements, indicating a relevant role in the MS pathogenesis. Among the available drugs to treat MS is Fingolimod (FING), an immunosuppressant that acts on sphingosine-phosphate receptors, which are found in several cells, including astrocytes.