Prenatal alcohol exposure (PAE) can lead to a variety of cognitive, behavioral, and health deficits throughout the life course falling under the umbrella of fetal alcohol spectrum disorder (FASD). The most common of these is depression, which impacts up to 50% of people with FASD. While the exact biological mechanisms placing individuals with FASD at increased risk for depression are unknown, previous studies have shown DNA methylation (DNAm) – a type of epigenetic modification – is a prime candidate.
We want to better understand the relationship between prenatal alcohol exposure and later depressive symptoms. Specifically, if there are particular trimesters in pregnancy where prenatal alcohol exposure may have a bigger impact on child DNAm and later depressive symptoms. Additionally, we want to understand the role of DNAm in linking prenatal alcohol exposure to increased risk for depression. We hope that through uncovering sensitive periods in development where PAE is most harmful and better understanding the role of DNAm in the relationship between PAE and depression, we can pave the way for more targeted interventions and treatments to reduce mental illness in people with FASD.
This research is funded by the National Institute of Alcoholism and Alcohol Abuse (NIAAA) and includes collaborations with researchers at Mass General Hospital (Dr. Erin C. Dunn) and the University of British Columbia (Dr. Joanne Weinberg).
The Lussier Lab 