Publication Date

Spring 2026

School

School of Health Sciences

Major

Biology: Biomedical Sciences

Keywords

prenatal maternal stress, fetal neurodevelopment, epigenetics, HPA axis, autism spectrum disorder, neurodevelopmental disorders

Disciplines

Developmental Biology | Developmental Neuroscience | Genetics and Genomics | Neuroscience and Neurobiology

Abstract

The hypothalamic-pituitary-adrenal (HPA) axis is the primary stress response system responsible for regulating cortisol release. During pregnancy, maternal stress can dysregulate the HPA axis, leading to elevated cortisol and corticosterone levels that impact fetal development. Excessive prenatal exposure to stress has been associated with alterations in fetal brain structure and function, increasing the risk for neurodevelopmental disorders such as autism spectrum disorder, attention-deficit/hyperactivity disorder, and anxiety. Emerging research supports the idea that these neurodevelopmental effects may be transmitted through epigenetic mechanisms. However, a gap remains in the literature regarding the specific mechanism of interaction between environmental stressors, heritable epigenetic information, and neurodevelopmental outcomes. This thesis elucidates the gap by discussing how maternal physiological stress systems contribute to adverse offspring neurodevelopmental outcomes, the impact of stress on epigenetic modulation, and which specific genes and epigenetic modifications have been associated with adverse outcomes in offspring exposed to prenatal stress.

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