Grant: CIHR Fellowship

It's estimated that 30 million children worldwide have faced significant hardships, such as maltreatment, loss of a parent, or living in poverty. These early life stressors (ELS) have been shown to increase an individual's lifelong risk of mood disorders such as depression and anxiety. The experience of ELS makes individuals more sensitive to stress as adults, which may explain why they are more prone to these disorders. Despite its importance to global mental health, we still don't fully understand the biological reasons behind this increased sensitivity to stress. Research suggests that changes in a reward centre brain region called the ventral tegmental area (VTA) may play a key role in ELS-related mood disorders. ELS seems to alter how this dopamine-producing brain region responds to stress and rewards, with studies in mice showing lasting changes in gene activity. This indicates that ELS might influence epigenetic processes-changes in gene expression triggered by environmental factors, such as the large stress hormone fluctuations elicited by ELS. My project aims to use cutting-edge techniques to reveal how ELS affects the chromatin - the structures that package DNA - in cells of the VTA during development. I then plan to uncover how these changes due to ELS lead to different patterns of neuron activation in response to adulthood stress. Finally, I aim to manipulate gene expression in the cells primarily affected by ELS to try and alleviate the adulthood stress-sensitivity caused by ELS. This work will serve as a vital foundation for understanding the long-term effects of ELS on brain development and function. By identifying specific molecular changes and pathways altered by ELS, this project will reveal novel targets for therapeutic interventions. Ultimately, it is my hope that these findings could lead to more effective treatments for mood disorders, tailored to individuals with a history of ELS.