Risk factors for the development of psychiatric disorders across development
Infancy is a period of expansive brain growth, and development. It is also a time of heightened sensitivity to external influences, some of which have long-lasting implications on neuronal structure and function. One such influence can be the quality of maternal caregiving received. Behavioral studies have also shown that infant emotion dysregulation is a risk factor for future behavioral or emotional problems. Little is known about the interplay between typical development of infant emotionality and brain measures. Finding biological correlates of temperament during infancy would better our understanding of brain-behaviour relationships, but may also be helpful in predicting future psychological outcomes. In this talk, I will share our current investigation of: (1) the relationship between infant emotionality and neural correlates related to diffusion tensor imaging and resting state connectivity network measures; and (2) the potential moderating effects of maternal caregiving on these relationships.
Relatedly, brain development continues during childhood and adolescence. This is also a period of high sensitivity to experience; where some negative experiences can have life-long implications on brain growth and development. Here, we were interested in investigating the specific contributions of genetic and environmental influences within a population particularly vulnerable to developing psychiatric disorders; children of parents diagnosed with Bipolar Disorder (BD). While the involvement of both genetic and environmental influences on the development of Bipolar Disorder (BD) is apparent, the individual importance and interplay between these two factors is unclear. Even less clear is understanding of how these factors influence functioning of emotion and reward processing neural networks in individuals most at risk of future BD. In this talk, I will share our findings of aberrant functional connectivity between the bilateral anterior cingulate cortex and the left ventrolateral prefrontal cortex with increased number of stressful life event exposure between offspring groups.