Mark Petersen

My research centers on vascular mechanisms of neurological disease with a particular focus on neonatal brain injury. Blood vessels become damaged in the injured or diseased brain which allows proteins from the blood to leak into the nervous system. My work seeks to identify new therapies for neurological diseases by targeting toxic blood proteins and inflammatory signals at the blood-brain interface that block normal brain development and repair. To achieve this goal, our group has developed a multifaceted research program incorporating basic science studies of stem cells and animal models with translational studies of human tissue and blood biomarkers. We have discovered critical links between blood coagulation, inflammation, and stem cell dysfunction in neurological disease. The nervous system has long been defined by its limited capacity for regeneration which results in persistent neurological deficits after nervous system damage. Stem cells are abundant in the brain, but why these stem cells are unable to fully restore neural tissue after injury has remained a mystery. We found that the blood clotting protein fibrinogen causes inflammation in the brain and blocks stem cells from becoming mature, myelin-repairing cells. We are now designing therapies to overcome the inhibitory environment in the damaged nervous system to promote regeneration and normal brain development. Through collaborations with the UCSF Preterm Birth Initiative and UCSF Newborn Brain Research Institute, we are also extending our studies to explore how maternal inflammation and coagulation contribute to preterm birth and poor neonatal outcomes. By combining large population datasets with state-of-the-art multiplex and proteomic approaches to measure blood biomarkers, we hope to identify druggable pathways at the maternal-fetal interface that can be targeted to prevent or lessen the impact of preterm birth and neonatal brain injury.