Gene-Environment Interactions on Brain Development
Our research focuses on how environmental exposure impacts early brain development, with a particular interest in the novel roles of the placenta. Specifically, our study is aimed:
- To identify new targets susceptible to environmental exposure in relevance with neurodevelopment
- To determine the roles of placenta/placental extracellular vesicles in the regulation of neurodevelopment in the absence and presence of environmental exposure
- To elucidate the link between genetic variability and neurodevelopmental outcomes
Disruption of neurodevelopment and cognitive function early in life due to environmental exposures can have lifelong impacts. The fetal period is a time of heightened vulnerability. Prenatal or postnatal exposure to environmental perturbation such as malnutrition, pollution, and heavy metals has been associated with low IQ and impaired neurobehavioral and cognitive functions. However, the molecular mechanisms by which environmental factors impact early brain development remain poorly understood.
Few studies have focused on fetal neuroprogramming as a result of the inter-relationships between neurotoxicants and the placenta. Placental trophoblasts actively release extracellular vesicles (EVs) into the maternal and the fetal circulation. EVs shuttle cargoes of bioactive molecules, such as proteins, lipids, and nucleic acids, from trophoblasts to the recipient cells, modifying gene expression and biology in the cells. Growing evidence indicates that EVs reach fetal neural cells after crossing the brain blood barrier. However, it is not known whether environmental exposure during pregnancy affects the production, release, and/or cargoes of placental EVs and how these changes lead to divergent neurodevelopmental outcomes.
To fill these knowledge gaps, we combine the advantages of the state of art -omics approaches, molecular mechanistic studies, and human genetic epidemiology in children. The long-term goal is to provide therapeutic strategies to prevent or reduce adverse neurological outcomes.