Causes of neurodegenerative diseases, such as multiple sclerosis (MS), have been attributed to an increase in oxidative stress, and this increased level of stress leads to the downregulation of the folate-vitamin B12 pathway. This downregulation inhibits gene expression by disrupting the methionine metabolism cycle, decreasing the amount of methylation occurring in cells. A possible mechanism that could be utilized to reduce the progression of MS is the induction of a separate methylation pathway independent from the folate-vitamin B12 cycle by using the enzyme betaine-homocysteine methyltransferase (BHMT), which methylates homocysteine back to methionine with betaine. BHMT is found in the nucleus of both primary neurons and oligodendrocytes and can influence gene expression. To test this hypothesis, we sought to examine how different treatments affect the way BHMT binds to chromatin to obtain a deeper understanding of how this alters gene expression. Specifically, we wanted to see the ways in which BHMT binding was altered through exposure to varying degrees of oxidative stress. This allowed us to identify which treatments caused BHMT to bind more tightly to the chromatin and therefore determine which of the conditions play the most important role in chromatin remodeling. Our data suggest these changes in gene expression are involved in MS pathology.