Neurodevelopmental disorders such as cerebral palsy and autism are common chronic childhood disorders with no effective cure. Half a million children under the age of 18 in the United States have cerebral palsy, and one in 6 children have some form of developmental disability. In term infants that suffer asphyxia at birth, low oxygen levels and low blood flow can cause hypoxic-ischemic encephalopathy, which is a major cause of cerebral palsy and related disabilities. Dr. Wilson’s research is focused on reducing brain damage in infants exposed to perinatal hypoxia-ischemia. Therapeutic hypothermia is the first intervention to reduce brain injury in term infants after perinatal asphyxia, but protection is typically incomplete and rates of mortality and severe disability remain high. There remains a critical need for complementary therapies that improve neuroprotection and address the negative effects of hypothermia and rewarming.

Dr. Wilson investigates molecular mechanisms of hypoxic ischemic injury in the developing brain and neuroprotective effects of drugs, hypoxic preconditioning, and hypothermia. She has investigated how changes in gene expression after a brief period of hypoxia reduce the vulnerability of the brain to a later, more severe HI insult. She also studies sex differences in brain injury mechanisms that are triggered by hypoxic ischemic injury in neonatal mice and has shown that there are sex-specific differences in the neuroprotective effects of some therapeutic interventions. Dr. Wilson’s current work investigates the neuroprotective mechanisms engaged by hypothermia in neonates, with the goal of developing complementary therapies that enhance hypothermic neuroprotection.

Dr. Wilson also collaborates with Dr. William Baumgartner and colleagues to study brain injury after hypothermic circulatory arrest (HCA). This research uses an animal model of this surgical intervention, which is used for complex repairs to the heart or major vessels in infants and adults. These studies have revealed inflammatory as well as apoptotic mechanisms that are activated after hypothermic circulatory arrest and have also identified serum biomarkers that can be used to detect brain injury early in the postoperative period. Studies in collaboration with Drs. Kannan Rangaramanujam and Sujatha Kannan recently showed that dendrimer nanoparticles can be used to deliver therapy to injured neurons and activated microglia after hypothermic circulatory arrest. This therapeutic approach holds great promise for prevention of brain injury after hypothermic circulatory arrest; Dr. Wilson and her colleagues are also investigating dendrimer nanotherapy for treatment of neonatal hypoxic-ischemic brain injury.