Introduction Multiple sclerosis (MS) is a devastating demyelinating disease that affects the central nervous system (CNS) and causes impairment of motor and sensory function (Karussis, 2014, p. 134) . MS is characterized by three main features: inflammation and subsequent demyelination and axonal damage (Karussis, 2014, p. 134). An inflammatory response begins when T cells attack myelin, recognizing self antigens as foreign (Karussis, 2014, p. 134). The inflammatory response propagates demyelination and axonal damage (Karussis, 2014, p. 135). An important cell involved in the pathogenesis of MS, oligodendrocytes (OL) are responsible for the creation of myelin (Zhang et al., 2009, p. 19162). MS patients have a reduced number of OLs, resulting in lower myelin production and reduced neural transmission speed (Karussis, 2014, p. 134). In the initial stages of the disease, remyelination occurs; however, as MS progresses, OLs become less capable of repairing the damage (Zhang et al., 2009, p. 19162). Notch1 and its ligand, Jagged1, have been identified as critical mediators of oligodendrocyte progenitor cell (OPC) recruitment and differentiation. (Zhang et al., 2009, p. 19162). OPCs are recruited to demyelinated axons, where they differentiate into OLs, producing myelin to remyelinate CNS axons (Jurynczyk & Selmaj, 2010, p. 7). Notch1 receptors are found on OPCs, and Jagged1 ligands are present on axons and adjacent glial cells (Woodhoo et al., 2009, p. 841). MS lesions have typically high numbers of Notch1 receptors; furthermore, Jagged1 is also abundant in MS lesions (Stidworthy et al., 2004, pp. 1931-1934). Interactions between Notch1 and Jagged1 result in the inability of OPCs to differentiate into OLs, in turn impairing the OPC...... middle of paper... p. 134). The Notch1/Jagged1 pathway is extensively involved in demyelination and, as such, is a therapeutic target for remyelination of CNS axons in individuals with MS (Zhang et al., 2009, p. 19162). Through a cascade of intracellular events, binding of Jagged1 to Notch1 induces suppression of transcription factors that prevent the differentiation of neural precursor cells into OPCs (Aparicio et al., 2013, p. 820). As a result, OPCs cannot undergo further maturation into OL, resulting in a reduced ability to repair demyelinated axons (Aparicio et al., 2013, p. 829). The Notch1/Jagged1 pathway is ideal as a therapeutic target for remyelination, as there are several steps that it can interfere with (Zhang et al., 2009, p. 19162). Impairment of the Notch1/Jagged1 pathway allows maturation of the OL and subsequent remyelination (Perez et al., 2013, p. 273).