Our research focuses on understanding the pathophysiology of brain injury in the neonatal period, which is a major contributor to mortality and lifelong morbidity. In our translational research group we study how early life events, like hypoxic-ischemic perinatal events, including birth asphyxia and perinatal stroke, or (extreme) preterm birth, lead to injury in the developing brain and how this impacts neurodevelopmental outcome on the long run.

Deciphering Early Brain Injury Mechanisms to Develop Neuroprotective Strategies for Newborns

Our team explores the pathophysiological cellular and molecular mechanisms of early brain injury in in vitro and in vivo models relevant for the target patient. In one of our research lines we try to decipher early damaging cascades after hypoxic-ischemic injury in the term brain. Understanding the intricate interplay between these detrimental cascades can aid in identifying novel targets to develop new strategies to combat neuronal brain injury in the newborn brain. We currently focus on targets within neuronal apoptotic cascades, mitochonadidrial key proteins and neuroinflammatory routes.

Advancing Models and Therapies for Brain Injury following Extreme Preterm Birth

In an additional research line, we focus on developing in vitro and in vivo models for brain injury after extreme preterm birth (i.e. encephalopathy of prematurity (EoP)) including cerebral organoids. We study the underlying pathophysiology of EoP which comprises of hypomyelination of the developing brain, maturational arrest of oligodendrocyte precursors, aberrant interneuron development and neuroinflammation. We currently investigate whether stem cell therapy, growth factor supplementation, human milk oligosaccharide supplementation or immunomodulation would be promising strategies to boost myelination in the preterm brain.

Image left: Brain of a rat exposed to fetal inflammation and postnatal hypoxia as a model for encephalopathy of prematurity, showing active microglia (red, Iba-1) and astrocytes (green, GFAP) in the hippocampus (neuronal nuclei in blue). Courtesy of Chantal Kosmeijer.

Image right: Cerebral organoid stained for proliferating cells (red, Ki67) and oligodendrocytes (green, Olig2), DAPI is used as nuclear counterstain. Courtesy of Myrna Brandt.