Advisory Committee Chair
Shin-Ichi Kano
Advisory Committee Members
Michael Sloane
Minae Niwa
Document Type
Thesis
Date of Award
1-1-2025
Degree Name by School
Master of Science (MS) Heersink School of Medicine
Abstract
Maternal immune activation (MIA) refers to the occurrence of an inflammatory immune response during any stage of pregnancy. This manifests as the upregulation of proinflammatory cytokines and can be caused by air pollution, obesity, or viral infection. When this occurs during the first trimester in humans, it increases the offspring’s susceptibility to developing neuropsychiatric disorders such as autism (ASD) and schizophrenia (SZ), in males more commonly than females. In addition to behavioral manifestations of neuropsychiatric disorders, metabolic syndrome (MetS) is a common comorbidity, defined as the co-occurrence of three or more symptoms including but not limited to hyperlipidemia, hypertension, and insulin resistance. While this may be the result of neuronal dysfunction in the hypothalamus, which regulates the body’s response to nutrients, the mechanism by which this may occur remains unclear. In this study, we explored oligodendrocyte precursors (OPCs) as potential mediators of neuronal function in the hypothalamus, as oligodendrocyte (OL) and myelin pathology have emerged as hallmarks of the impaired neural communication seen in ASD and SZ. We aimed specifically to analyze OPCs, as myelinating OLs are not present in the brain at the time in development when MIA is induced, or during the first trimester of human pregnancy. Our hypothesis that MIA induces damage to OPCs in a sex and region-specific manner outlines one way in which MIA differentially affects male and female offspring, providing further evidence for the role of glial cells in neuropsychiatric disorders and their comorbidities.
Recommended Citation
Miller, Kate, "Maternal Immune Activation Causes Oligodendrocyte Deficits in the Hypothalamus" (2025). All ETDs from UAB. 6872.
https://digitalcommons.library.uab.edu/etd-collection/6872
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