We have found that transient prenatal hypoxia leads to long-term deficits in seizure threshold and other behavior anomalies without significant cell death or gross neuroanatomic injury. Therefore, we posit that these lasting functional injuries are due to disruption of the epigenome during critical periods of development.

Since the developing brain is a complex network of many types of neurons, glial, and endothelial cells, we are employing single-cell RNA and ATAC sequencing at the time of injury and cell type-selective conditional knockout models and viral vectors to identify candidate epigenetic modulators and directly study whether these candidate genes modulate neurodevelopment outcomes from prenatal hypoxia.

Many interesting directions have emerged. Please contact us if you want to join our team!