The CANDLab bridges clinical, developmental, and neuroscience approaches to better understand how the brain develops during childhood and adolescence and how these changes affect the development of emotional learning and regulation and risk for psychiatric illness. The majority of psychiatric disorders emerge during development, yet much remains unknown about how key neural circuits mature in normative development and how these processes go awry. Our lab aims to characterize frontolimbic trajectories across development, elucidate how early environments (e.g., early-life stress) and genetic factors influence sensitive periods in neurodevelopment and risk for psychopathology, and translate knowledge of brain development to optimize clinical interventions for anxiety and stress-related disorders in childhood and adolescence. These investigations have critical implications for understanding developmental changes in emotional learning and regulation that may promote resilience or increase risk at distinct developmental stages and for the early identification and treatment of psychiatric disorders.
Childhood and adolescence are marked by dynamic changes in emotional learning and regulation. Interactions between limbic and cortical brain structures and connectivity underlie the development of these fundamental affective behaviors and play a central role in emotional learning and regulation in adulthood. However, relatively little is known about the developmental construction of this circuitry in humans. Disruption in the development of connections between regions such as the amygdala and prefrontal cortex can lead to altered emotional behavior and may increase risk for myriad psychiatric disorders at unique stages of development. This line of research seeks to delineate the normative developmental trajectory of frontolimbic circuitry and related changes in emotional learning and regulation, as well as to serve as an important foundation for studies of the many clinical populations in which this circuitry is implicated.
Stress is a potent environmental risk factor for the onset and exacerbation of many psychiatric disorders, and stress that occurs early in life can have especially profound and lasting consequences on behavior. Prior research suggests that the amygdala is particularly vulnerable to stress, which may relate to the persistence of altered emotional phenotypes following early-life stress. We are currently investigating how early experiences affect neurodevelopment and emotional behavior, with a focus on how individual differences, the timing and nature of traumatic events, and coping responses influence risk versus resilience and inform early intervention strategies. We also seek to identify sensitive periods, during which the environment has particularly strong influences on neurodevelopment and thus lasting effects on behavior, as a powerful way to understand mechanisms of change with the emergence of psychopathology and when clinical interventions can be most effective.
The majority of psychiatric disorders emerge during the course of development, and anxiety disorders are the most common psychiatric illness among children and adolescents. Applying knowledge of typical and atypical frontolimbic and behavioral development can provide critical insight into neurodevelopmental pathways to anxiety and stress-related disorders and how to best treat these disorders in youth. In this line of research we are examining developmental changes in processes such as fear learning and emotion regulation that underlie anxiety disorders and how brain development might contribute to risk for anxiety at distinct developmental stages. We are interested in the central role that parents play in modulating how children learn about their environments and how they respond to fear, as well as the role that parents play in treatments for anxiety. Ultimately, we aim to translate studies of basic developmental affective neuroscience to inform innovative therapies and preventive strategies for anxiety disorders as a function of age, environmental, and genetic factors.