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.
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
- TrkB signaling and hypoxia-ischemia induced retinopathy