Objective: Multiple sclerosis (MS) is an inflammatory demyelinating disorder of the central nervous system. Currently available MS treatments focus on the modulation of inflammation and do not directly address the key disease process of demyelination, although remyelination is essential to prevent progressive axonal injury and subsequent neurodegeneration. Identification of new players in the pathology of MS may therefore help design novel therapies aimed at promoting remyelination. The main objective of this study was to gain further insights into the molecular mechanisms underlying progressive MS pathogenesis, in order to identify novel therapeutic targets.