Decoding the Spatial Architecture of Newborn Brain Injury
Infants born early (preterm) are at risk for brain injury and long term neurodevelopmental challenges, including delays in walking, language development, and school-aged cognitive performance. Preterm brain injury is complex, but a major contributor to abnormal brain development is chronic exposure to low oxygen (hypoxia) due to lung immaturity. We know from prior work that specific brain cell populations (oligodendrocytes) that are responsible for myelination are injured in the preterm brain, but we do not understand why or how. In this work, we will use advanced imaging and genomics to map the developmental and sex specific trajectory of brain injury and recovery in a mouse model of preterm brain injury. We will discover mechanisms by which normal cellular communication goes awry in preterm brain injury, and we will validate our findings in human brain tissue. Based on our preliminary data, we will test whether a therapy targeting a specific pathway in oligodendrocytes can improve outcomes in mice with hypoxic brain injury. In total, this work will greatly expand our knowledge of the biology of brain injury in preterm infants and open avenues to investigate new targets for therapy to improve the lives of these fragile newborns.
Brian Kalish , The Hospital for Sick Children
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