Cengiz Research Group

Dr. Pelin Cengiz’s research focuses on finding a novel therapy for neonatal encephalopathy subsequent to hypoxia ischemia (HI). She uses the experimental (Vannucci-Rice) mouse model of hypoxia ischemia (HI) to study the sexually differentiated role of neurotrophin signaling in the neonatal hippocampus post-HI.  The neurotrophin receptor, tyrosine kinase B (TrkB), plays an important role in neuroprotection and improving the long-term functional recovery following cerebral ischemia by increasing neuronal survival. She has shown that administration of 7,8 dihydroxyflavone (7,8-DHF; potent and selective TrkB agonist) increases TrkB phosphorylation and hippocampal neuronal survival following HI in female, but not in male newborn mice. This female-specific responsiveness to TrkB agonist therapy mimics improved outcomes observed clinically in female newborn humans post-HI. Her studies focus on the cellular mechanisms of the female-specific responsiveness to TrkB agonist and their roles in improving long-term neurological and functional outcome post-HI. An improved understanding of the cellular mechanisms that underlie sex-specific neurotrophin responses will identify new avenues for developing novel therapeutics for neonates and children suffering from brain injury.

Study Led By Pelin Cengiz, MD, Examines Why Female Newborns are Better Protected from Brain Injury

As a University of Wisconsin former ICTR KL2 scholar, the Clinical and Translational Research Training was crucial in retooling her lab after her primary research mentor left UW-Madison in 2011. With the support of the KL2 Program, Cengiz was able to expand her mentoring team and continue to move her research project forward without a lapse in productivity.

Dr. Cengiz’s clinical duties include serving as an Attending in the PICU and in the Outpatient Sedation Clinic at American Family Children’s Hospital. Abroad, she is an active member of the international health community.

Additional Research Activities

• Role of estrogen receptors and TrkB signaling in sexed hippocampal astrocytes and neurons after in-vitro ischemia
• TrkB signaling in sex specific hypothermic neuroprotection
• Sex specific protective effects of 7,8 DHF on learning and memory after HI
• TrkB signaling and hypoxia-ischemia induced retinopathy