How do we become who we are?
One of the major questions driving the field of developmental neuroscience is “How do we become who we are?” This question is one of the most intriguing, and incidentally, one of the most complicated to address. Part of the complication arises from the fact that each individual encounters unique experiences throughout his or her life course that can have profound impacts on the brain and, consequently, behavior.
Our primary research interests focus on the biological mechanism underlying neurobehavioral deficits induced by pre- and/or postnatal adverse experiences, with a special focus on the associated increased predisposition for developing psychopathologies such as depression and anxiety.
Prenatal Alcohol Exposure
Fetal Alcohol Spectrum Disorder (FASD) is one of the most prevalent neurodevelopmental disorders—up to 4% prevalence in Canada—and encompasses a wide-range of physical, physiological, and neurobehavioral changes resulting form prenatal alcohol exposure (PAE).
Individuals prenatally exposed to alcohol also show dramatically higher rates of mental health problems, including depression and anxiety. The underlying mechanisms mediating these increased rates of mental health problems following PAE are not completely understood. However, the immune system is increasingly recognized as playing an important role in typical brain development and function, and immune dysregulation is known to occur in individuals with depression and anxiety.
Using a translational approach to explore parallel and complementary outcomes in an animal model of PAE and human cohorts of individuals with FASD, our research is investigating the possibility that PAE-induced changes in immune function may underly the increased vulnerability to mental health problems following PAE.
We have known for many years that exposure to early-life adversity, such as abuse, maltreatment, and/or neglect significantly increases the risk for later mental health problems, including depression and anxiety. Yet, we still have little understanding of how the infant brain responds to adversity and which specific factors within the complex social trauma initiate negative developmental trajectories leading to later life pathology.
Our research uses multiple animal models of early-life adversity to systematically identify key factors that are sufficient and necessary to induce adversity-related neurobehavioral deficits.