Epigenetic
organization of juvenile brain and behavior: Do sex differences in
neuroepigenetic mechanisms mediate risk or resilience to the impact of
early-life adversity on juvenile mental health disorders?
Overview of Research
Interests:
The study of epigenetics allows for the understanding of how early gene x
environmental interactions can shape lasting differences in gene function and
behavior. As such, juvenile social disorders may result from atypical epigenetic
programming of neuronal tissues during critical periods of development. To
investigate the epigenetic programming of juvenile social disorders, my
research has focused on how brief environmental perturbations in epigenetic
processes within the developing brain can have lasting consequences on juvenile
social behavior and health disparities. As
some juvenile mental health disorders are diagnosed at different rates between
males and females, we are examining how sex differences in epigenetic processes
underlie risk and resilience to some mental health disorders.
Neuroepigenetic programming of juvenile rat social behavior as a model for sex differences in risk or resilience to developmental neuropsychopathology
Sexually dimorphic
risk and resilience
Although there are physiological and behavioral differences between men and women, perhaps the most profound sex differences are in neurological and psychiatric disorders. Sex differences have been reported in depression, schizophrenia, autism, and attention-deficit hyperactivity disorder. Currently, it is unclear how these differences occur and to what extent they are different between men and women. My research suggest that environmental and hormonal influences during development may produce sex differences in the epigenome, and that these differences play an important role in gating risk or resilience to a number of neurological and psychiatric disorders.
Our own data indicate that epigenetic processes play an important role in programming the juvenile social brain. The dynamic interaction between epigenetic factors and chromatin leads to functional plasticity within the brain that may explain the diversity of responses to endogenous and exogenous signals later in life. Subtle variations in these epigenetic factors may also partially explain individual differences in the development of neurological and mental health disorders. We propose that sex differences in these epigenetic factors not only contribute to sexual differentiation of the brain, but that they also confer sexually dimorphic risk and resilience for developing neurological and mental health disorders later in life. In particular, we are examining how epigenetic mechanisms within the developing amygdala control typical juvenile social development.
Although there are physiological and behavioral differences between men and women, perhaps the most profound sex differences are in neurological and psychiatric disorders. Sex differences have been reported in depression, schizophrenia, autism, and attention-deficit hyperactivity disorder. Currently, it is unclear how these differences occur and to what extent they are different between men and women. My research suggest that environmental and hormonal influences during development may produce sex differences in the epigenome, and that these differences play an important role in gating risk or resilience to a number of neurological and psychiatric disorders.
Our own data indicate that epigenetic processes play an important role in programming the juvenile social brain. The dynamic interaction between epigenetic factors and chromatin leads to functional plasticity within the brain that may explain the diversity of responses to endogenous and exogenous signals later in life. Subtle variations in these epigenetic factors may also partially explain individual differences in the development of neurological and mental health disorders. We propose that sex differences in these epigenetic factors not only contribute to sexual differentiation of the brain, but that they also confer sexually dimorphic risk and resilience for developing neurological and mental health disorders later in life. In particular, we are examining how epigenetic mechanisms within the developing amygdala control typical juvenile social development.
Chromatin
remodeling and the development of typical juvenile social behavior
Our research illustrates how subtle alterations of epigenetic proteins within the developing amygdala can have enduring consequences on juvenile social and anxiety-like behavior. We are currently investigating the epigenetic programming of genes that confer risk to both autism and schizophrenia-spectrum disorders. As such, we are finding sex differences in DNA promoter methylation patterns of genes implicated in both autism and schizophrenia spectrum disorders. These data may help elucidate why males are at greater risk for early diagnoses of autism and schizophrenia. We are examining the lasting consequences of disturbances in the expression and function of these genes within the developing amygdala on juvenile social and anxiety behavior.
In summary, we are examining how early-life adversity alters the epigenetic programming of genes that confer risk or resilience to mental disorders using both human and rodent models.
Our research illustrates how subtle alterations of epigenetic proteins within the developing amygdala can have enduring consequences on juvenile social and anxiety-like behavior. We are currently investigating the epigenetic programming of genes that confer risk to both autism and schizophrenia-spectrum disorders. As such, we are finding sex differences in DNA promoter methylation patterns of genes implicated in both autism and schizophrenia spectrum disorders. These data may help elucidate why males are at greater risk for early diagnoses of autism and schizophrenia. We are examining the lasting consequences of disturbances in the expression and function of these genes within the developing amygdala on juvenile social and anxiety behavior.
In summary, we are examining how early-life adversity alters the epigenetic programming of genes that confer risk or resilience to mental disorders using both human and rodent models.