March 19, 2024

Jessica L. Bradshaw, PhD 

Dr. Jessica Bradshaw is a Postdoctoral Research Associate completing her postdoctoral training in neuroendocrinology, behavior, and rodent models of intermittent hypoxia under the primary mentorship of Dr. Rebecca Cunningham at the University of North Texas Health Science Center in Fort Worth, Texas. Dr. Bradshaw was classically trained as an immunologist during her graduate studies and combines this expertise and experience with her research interests in maternal cardiovascular and brain health during pregnancy and post-pregnancy. Her postdoctoral studies were supported by an American Heart Association postdoctoral fellowship examining the role of innate immune activation in preeclampsia, a hypertensive disorder of pregnancy. Dr. Bradshaw’s current studies are focused on the intersection of hypoxia and inflammatory processes in maternal brain health during pregnancy and the postpartum period. Her research has contributed to our understanding of the impact of gestational immune activation on maternal cardiovascular outcomes and fetal growth dynamics, as well as maternal brain plasticity and behavior during pregnancy and post-pregnancy. Dr. Bradshaw is a tireless advocate for women’s health research and maternal health equity and enjoys spending time with her four children, two dogs, and supportive spouse.


Abstract: Pregnancy-associated Oxidative Stress and Inflammation are not Associated with Impaired Maternal Neuronal Activity or Memory Function 

Jessica L. Bradshaw [1], E. Nicole Wilson [1], Jennifer J. Gardner [1], Steve Mabry [1], Selina M. Tucker [1], Nataliya Rybalchenko [1], Edward Vera Jr. [1], Styliani Goulopoulou [2], Rebecca L. Cunningham [1].  

[1] UNT Health Science Center, Fort Worth, Texas, USA  

[2] Loma Linda University, Loma Linda, California, USA 

Pregnancy is associated with neural and behavioral plasticity, systemic inflammation, and oxidative stress. The impact of inflammation and oxidative stress on maternal neural and behavioral plasticity are unclear. We hypothesized that the maternal hippocampal CA1, a brain region associated with cognition, would be protected from pregnancy-associated inflammation and oxidative stress, mediating stable peripartum cognitive performance. Cognition was tested using novel object recognition, Morris water maze, and open field behavior tasks in nulliparous (nonpregnant), pregnant (near term), and primiparous (two-months post-pregnancy) Sprague-Dawley rats. Plasma and CA1 proinflammatory cytokines were measured via MILLIPLEX magnetic bead assay. Plasma oxidative stress was measured via advanced oxidation protein products assay. CA1 markers of oxidative stress, neuronal activity, and apoptosis were quantified via western blotting. Our results demonstrate CA1 oxidative stress was elevated in pregnant compared to nulliparous rats but was equivalent levels in pregnant and primiparous rats. Reproductive state did not impact CA1 inflammatory cytokines, neuronal activity, apoptosis, or memory function. Spatial learning was impaired while anxiety-like behavior was reduced in primiparous rats. Our data highlight long-term effects of pregnancy on maternal cognitive performance and suggest maternal hippocampal CA1 is protected from systemic inflammation but vulnerable to peripartum oxidative stress. Funding: NIH R01 HL146562, T32 AG020494; AHA 903250, 9