Analysis of Neurogenic Response in a Viral Model of Multiple Sclerosis

Multiple Sclerosis (MS) affects nearly 400,000 Americans and every hour someone is newly diagnosed. Worldwide, MS affects roughly 2.1 million people. As of today, there are pharmaceutical agents that are used to relieve symptoms of MS, yet none are able to stop disease progression. There still is the question of how to potentially cure MS. Currently, big hopes have been deposited on using neural stem cells (NSCs) to treat MS patients. Overall, MS cases are distinguished by chronic progressive evolution with relapsing remitting episodes of demyelination/remyelination. The remission phase is where there have been attempts done, potentially with the aid of NSCs, to remyelinate.

In order to progress towards a cure for this disease, we focused on investigating the mechanisms that mediate the lack of repair in MS. For this, we utilized a mouse viral model of MS, known as Theiler’s Murine Encephalomyelitis Virus (TMEV). SJL mice are susceptible to the infection of this picornavirus. In these mice, TMEV is known to induce a demyelinating disorder similar to the pathology of MS. With this model, we studied changes in the neurogenic region of the brain 7 and 30 days post-infection Immunohistochemistry and stereology techniques were used. We found that TMEV infection directly affects neurogenesis from NSCs and induces apoptosis. Based on our findings, we concluded that TMEV infection does chronically progress and affects endogenous neurogenesis. This will help us further understand how to potentially stimulate efficient myelination in MS, thus, leading to the progression of more effective therapies for MS.