Abstract: Multiple sclerosis (MS) is a chronic inflammatory and demyelinating disease of the central nervous system (CNS). Patients with MS experience sensory and motor function loss due to myelin and/or axon damage perpetuated by infiltrating immune cells (Hauser and Cree, 2020). Before modern therapies, most patients experienced heightened symptoms followed by partial recovery. A significant proportion of these patients would then advance to a progressive disease state which features continual neuroaxonal loss and less frequent recovery (Degenhardt et al., 2009). However, with the advancement of several treatment strategies, the view of MS within the field has also begun to evolve. Current therapies reduce or eliminate the occurrence of relapse, yet there is still progression independent of relapse activity (Tur et al., 2023). These treatments prevent relapses primarily by limiting new lesions formed by the infiltration of T cells, B cells, and macrophages from the periphery, inciting inflammation and myelin damage. Newly formed lesions are often called active lesions due to their inflammatory nature. Ocrelizumab, which depletes CD20+ B cells, and Natalizumab, which targets the α4-integrin subunit of α4β1 to hinder lymphocytes from entering the CNS, are examples of commonly used treatments to prevent active lesion formation (Hauser and Cree, 2020).