Epigenetic Signatures of War and Conflict-Related Trauma - A Study of Refugee Families in Africa
The number of refugees in the world has reached more than 25 million people. General estimates show high prevalence rates of mental health problems, such as posttraumatic stress disorder (PTSD), among refugees. Understanding the psychological and biological underpinnings of behavioral vulnerability and resilience to traumatic stress is a public health priority, as it would facilitate the development of targeted preventative strategies and therapeutic interventions. Extensive evidence shows a link between exposure to war- and conflict-related trauma and increased risk for psychopathology. However, there exists significant variability in PTSD prevalence following trauma exposure. The development of PTSD is thought to result from the interaction between environmental and personal risk factors (i.e., trauma exposure and genetic risk). One mechanism for gene by environment interactions that differentiates risk vs. resilience is via epigenetic processes. However, compelling human evidence linking trauma exposure and/or trauma-related psychopathology to specific epigenetic alterations remains sparse. This is partly due to design limitations and the fact that the majority of studies has so far focused on candidate genes with low coverage across genes, which might miss important differentially methylated genomic regions, and there are currently few epigenome-wide studies. Thus, no clear picture of an epigenetic PTSD signature has emerged so far.
In this project, we will investigate a well-characterized sample of Burundian refugee families exposed to multiple severe trauma and resettled in three refugee camps in Tanzania using state-of-the-art array-based technology to explore PTSD symptom related alterations across the genome. Our sample is particularly suitable for studying the interplay of traumatic experiences, trauma-related disorders, and potential epigenetic mechanisms due to its homogeneity in terms of ethnic background and current living situation, and high levels of exposure to war- and conflict-related violence. We aim to identify PTSD-associated alterations of DNA methylation that distinguish between individuals who developed PTSD following war-related trauma exposure and unaffected individuals with the same exposure. We further aim to show that trauma load is related to DNA methylation patterns. Lastly, we aim to demonstrate the mediating role of DNA methylation in the association between trauma exposure and PTSD risk. In addition, we aim to confirm our findings using existing validation samples.
Contact M.Sc. Katharina Mattonet
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