Postdoctoral Scholar

Neonatal Hypoxic – Ischemic (HI) Encephalopathy is one of the most devastating conditions that can occur during the perinatal period, with therapeutic hypothermia (TH) being the only legitimate treatment option available to clinical practice. Still, the rate of death or disability after TH remains unacceptably high (60%).

My current research concentrates on investigating the metabolic state of the hypoxic neonatal brain and discovering hints or “metabolic fingerprints” that can identify responders and non-responders to TH. Using the breakthrough technology of hyperpolarized carbon (HP¹³C) spectroscopy combined with the traditional proton magnetic resonance spectroscopy (¹H-MRS) we can not only look at the steady pool of metabolites but also measure reaction rates and dynamic changes in metabolic conversion during cerebral hypoxia.

To better understand the cellular events that take place during and after a hypoxic ischemic insult, we moreover employ a cell-biological approach. One of the key elements of the downstream signaling that takes place in HI is the transcription factor HIF-1. HIF-1 regulates the switch from oxidative to glycolytic metabolism under hypoxic conditions and plays an instrumental role in cell fate commitment. The advent of the CRISPR/Cas9 technology allows us to efficiently silence the HIF-1 gene in individual neuron and astrocyte populations or in their co-cultures and evaluate the consequences of such a deletion.

Using the metabolic and cellular data to identify vulnerable pathways allows for the design of novel, unique treatments and better management of the newborns who are less likely to respond to the standard therapeutic strategies.