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Rachel E. Chase, Ph.D.

Visiting Assistant Professor
Rachel Chase smiling in front of an exposed brick wall.


  • B.A. (Neuroscience, summa cum laude) - Wartburg College
  • B.A. (French and Francophone Studies, summa cum laude) - Wartburg College
  • Ph.D. (Neuroscience) - University of Iowa

Courses Taught

  • PY 222 - Cognitive Psychology
  • PY 291 & 292 - Research Methods I and II
  • PY 420 - Neuropsychology of Nutrition


  • Schroeder, R. E., Nguyen, L., Pieper, A. A., & Stevens, H. E. (2022). Maternal treatment with P7C3-A20 protects from impaired maternal care after chronic gestational stress. Behavioural Brain Research, 416, 113558. [doi]
  • Schroeder, R., Sridharan, P., Nguyen, L., Loren, A., Williams, N. S., Kettimuthu, K. P., Cintrón-Pérez, C. J., Vázquez-Rosa, E., Pieper, A. A., & Stevens, H. E. (2021). Maternal P7C3-A20 treatment protects from neuropsychiatric sequelae of prenatal stress. Antioxidants & Redox Signaling, 35(7), 511-530. [doi]
  • Dowell, J.*, Elser, B. A.*, Schroeder, R. E.*, & Stevens, H. E. (2019). Cellular stress mechanisms of prenatal maternal stress: Heat shock factors and oxidative stress. Neuroscience Letters, 709, 134368. [doi]

*denotes shared first authorship

Areas of Specialization

During my graduate work, I used a mouse model to investigate how prenatal stress affects the neurodevelopment of the growing fetus. I also addressed changes to maternal depressive-like and anxiety-like behavior both pre- and postnatally, as well as repercussions on maternal care behaviors after birth. Because stress increases the production of reactive oxygen species (ROS) in both the stressed animal and in the fetal brain itself, I administered the ROS-reducing experimental compound P7C3-A20 to dams receiving prenatal stress to discover whether it could rescue the detrimental effects of stress on both fetus and dam.

For my postdoctoral research, I used the CRISPR CAS9 gene-editing system in cell culture to knock out the expression of various mitochondrial carboxylate fuel carriers in order to elucidate the cause of succinate buildup during ischemia (e.g., stroke). When tissue is reperfused following ischemia, the rapid oxidation of succinate causes a burst of ROS production, causing further cellular damage. The aim of my project was to identify which carrier(s) are responsible for succinate buildup in order to prevent it, and thus, prevent further injury upon reperfusion. In future work, I aim to combine my two areas of expertise - neuroscience and metabolism - and move into the field of neurometabolomics.