The goal of our collaborative work is to identify the cellular and epigenetic mechanisms whereby adult microglial activities are reprogrammed by early life exposures.

Microglia (resident CNS immune cells) play critical roles in virtually all aspects of brain health and disease by performing surveillance, inflammatory, and neuronal supportive activities, functions between which microglia readily and appropriately shift in the healthy CNS. However, our work has shown that these normal microglial activities become detrimentally (epigenetically) reprogrammed by early life exposures like in utero exposure to maternal sleep disordered breathing, such that microglia then contribute to neuronal degeneration and CNS pathology in adulthood. These disorders include cognitive/behavioral impairments, deficits in respiratory neuroplasticity, and cardiovascular dysfunction. Our studies are aimed at understanding the molecular underpinnings of these neural deficits in adulthood.