Defense Date
2026
Document Type
Thesis
Degree Name
Master of Science
Department
Anatomy & Neurobiology
First Advisor
Jeffrey L. Dupree
Abstract
Multiple sclerosis (MS) is a chronic autoimmune disease characterized by demyelination, neuroinflammation, and progressive neurodegeneration. Previous studies using the experimental autoimmune encephalomyelitis (EAE) model have reported that inflammation disrupts the axon initial segment (AIS), closely associated with microglial activation. It has been established that chronic stress disrupts glucocorticoid signaling, creating a primed state in which the immune system is activated to prepare for future dangers. My hypothesis is that exposure to chronic stress during adolescence prior EAE induction, will result in increased inflammation impacting clinical onset and severity, consequent to reactive microglia, which will be accompanied by a disruption in both AIS length and number. Twenty-eight mice were divided into four groups: Naïve, Stress Only, EAE Only, and Stress + EAE. EAE disease severity was assessed by recording clinical scores and clinical onset day. AIS structural integrity (quantified by AIS length and number) and microglial activation (quantified by morphological parameters) were analyzed using ImageJ. No significant difference was detected between EAE Only and Stress + EAE groups in clinical scores or clinical onset day, AIS number, or length, or in the six morphological/fractal parameters. Contrary to our initial hypothesis, chronic adolescent stress prior to disease induction did not increase disease severity.
Rights
© The Author
Is Part Of
VCU University Archives
Is Part Of
VCU Theses and Dissertations
Date of Submission
5-5-2026