| Abstract |
Multiple sclerosis (MS) is an autoimmune disorder characterized by demyelination of the central nervous system (CNS) and neurodegeneration. Serotonin is a neurotransmitter that plays a role in numerous pathways throughout the body including sleep, happiness, and epigenetic modifications. Recent studies have found that serotonin levels are decreased in MS for reasons that are currently unknown. This is significant because serotonin plays a role in the post-translational modification of histone 3. Because serotonin is decreased, we have hypothesized that serotonylation is decreased which leads to subsequent aberrant gene expression in MS. The purpose of this experiment is to explore a new epigenetic mark and its role in neurodegeneration and MS. Using the cuprizone mouse model of MS, we isolated brain tissue and looked at changes in serotonylation. Because Alzheimer’s disease (AD) is also characterized by neurodegeneration, brain tissue from mice treated with APP (AD mouse model) was also analyzed. Analysis was conducted on nuclear fractions via Western Blotting, confocal imaging, and densitometry.
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| Modified Abstract |
Multiple sclerosis (MS) is an autoimmune disorder characterized by demyelination of the central nervous system (CNS). In addition to its role as a neurotransmitter, serotonin also plays a role in epigenetic modifications. Recent studies have found that serotonin levels are decreased in MS for reasons that are currently unknown. This is significant because serotonin plays a role in modifying histone 3. Because serotonin is decreased, we have hypothesized that serotonylation, a post-translational modification, is decreased which leads to subsequent aberrant gene expression in MS. Using the cuprizone mouse model of MS and the APP mouse model of AD, we isolated brain tissue and looked at changes in serotonylation. Methods used to view these changes were Western Blotting, confocal imaging, and densitometry.
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