Rose M. De Guzman is a postdoctoral fellow in Dr. Andrea Edlow’s Lab at Massachusetts General Hospital. She received her BS in Nutritional Biochemistry at UC Davis, CA and earned her PhD in Behavioral Neuroscience at University at Albany, NY. Her scientific passions include nutrition, neuroscience, sex differences, pregnancy/postpartum, and child development.

Her PhD dissertation investigated how sexually dimorphic brain regions involved in maternal and stress circuitries change during the postpartum period. Her postdoctoral research studies the impact of maternal immune activation in pregnancy, including maternal obesity and COVID-19 infection, on fetal brain development and behavior. Her long-term goal is to develop personalized therapeutics, guided by patient-level biology.

Outside of lab, she is the founder of Women in Neuroscience and is involved in organizations that empower students, especially those with similar background of being low SES, first-gen college student, and an immigrant. She believes a diverse scientific community broadens scientific innovation. She also enjoys hiking, mountain biking, cooking, and concert/fashion photography.

Placental macrophages and umbilical cord blood mononuclear cells as a proxy cell type of microglia and a model for the impact of maternal COVID-19 on brain microglial activation

In collaboration with Dr. Andrea Edlow and Dr. Roy H. Perlis, we are using personalized microglial-like cellular models derived from cord blood monocytes to investigate the potential impact of maternal SARS-CoV- 2 exposure on fetal and offspring neurodevelopment. This work dovetails nicely with Dr. Edlow’s R01, examining fetal placental macrophages (Hofbauer cells) as a proxy cell type for fetal brain microglia in the setting of maternal obesity. Both projects are based on the premise that maternal inflammation may have deleterious effects on fetal brain macrophages (microglia). Microglia play a key role in modulating synaptic pruning, neurogenesis, phagocytosis of apoptotic cells, and regulation of synaptic plasticity. They can also be critical mediators of neurodevelopmental morbidity in maternal immune activation. To date, there is no biomarker or model for in utero microglial priming and function that might aid in identifying the neonates and children most vulnerable to neurodevelopmental morbidity, given that fetal and infant microglia remain inaccessible.

We will use umbilical cord blood mononuclear cells to reprogram induced microglial cells and to model phagocytic activity of these cells. Dr. Perlis and his laboratory developed and validated an approach for the transdifferentiation of human microglia-like cells from peripheral blood mononuclear cells (PBMCs) and assaying them with isolated synapses (synaptosomes) derived from neural cultures differentiated from induced pluripotent stem cells (iPSCs). For this project, however, the cord blood-based method is more rapid and scalable compared to the iPSC microglia method. This proposed method also enables investigation of epigenetic effects otherwise lost in iPSC generation, in addition to recapitulating morphology, transcriptome, and function of microglia.