Maternal preconception stress produces sex-specific effects at the maternal:fetal interface to impact offspring development and phenotypic outcomes†.

Entering pregnancy with a history of adversity, including adverse childhood experiences and racial discrimination stress, is a predictor of negative maternal and fetal health outcomes. Little is known about the biological mechanisms by which preconception adverse experiences are stored and impact future offspring health outcomes. In our maternal preconception stress (MPS) model, female mice underwent chronic stress from postnatal days 28-70 and were mated 2 weeks post-stress.

Chemogenetic activation of CRF neurons as a model of chronic stress produces sex-specific physiological and behavioral effects.

Trauma and chronic stress exposure are the strongest predictors of lifetime neuropsychiatric disease presentation. These disorders often have significant sex biases, with females having higher incidences of affective disorders such as major depression, anxiety, and PTSD. Understanding the mechanisms by which stress exposure heightens disease vulnerability is essential for developing novel interventions.

Extracellular vesicles are dynamic regulators of maternal glucose homeostasis during pregnancy.

Homeostatic regulation of the maternal milieu during pregnancy is critical for maternal and fetal health. The placenta facilitates critical communication between maternal and fetal compartments, in part, through the production of extracellular vesicles (EVs). EVs enable tissue synchrony via cell-cell and long-distance communication and are at their highest circulating concentration during pregnancy.

Elevated MeCP2 in Mice Causes Neurodegeneration Involving Tau Dysregulation and Excitotoxicity: Implications for the Understanding and Treatment of MeCP2 Triplication Syndrome.

Expression of MeCP2 must be carefully regulated as a reduction or increase results in serious neurological disorders. We are studying transgenic mice in which the MeCP2 gene is expressed at about three times higher than the normal level. Male MeCP2-Tg mice, but not female mice, suffer motor and cognitive deficits and die at 18-20 weeks of age.