Karestan Chase Koenen

This study fine-maps PTSD GWAS data with amygdala eQTLs and shows FOXP2 expression is linked to increased PTSD risk, with functional validation in mice and humans.

The paper investigates DNA methylation mediation between PTSD severity and cardiovascular disease risk, identifying six CpGs as potential epigenetic biomarkers.

This paper conducts a trans-ancestry GWAS of hot flashes, identifies TACR3 as a key genetic target, and finds genetic overlaps with psychiatric disorders.

The paper identifies five genomic factors explaining most genetic variance across 14 psychiatric disorders and finds shared and disorder-specific genetic signals with distinct biological functions.

The paper introduces BGE, a sequencing method that combines low-pass whole genome and deep whole exome data, showing high accuracy and cost-effectiveness for genetic variant discovery.

This study examines genetic structure in African populations using ethnolinguistic data, finding that language classifications better capture genetic variation than geography alone.

The paper develops a heterogeneous mediation analysis method to study DNA methylation's role in PTSD among African Americans, identifying subgroups and mediators linked to PTSD symptoms.

The paper examines how DNA methylation at NFATC1 CpG sites mediates the relationship between different trauma types and PTSD risk in a prospective study.

The paper examines associations between childhood family emotional health, brain grey matter volume, and DNA methylation in saliva, finding mediation effects and enriched biological pathways.

This study shows low-coverage sequencing is more accurate and cost-effective than GWAS arrays for detecting genetic variation in diverse African populations.

This study examines how neighborhood conditions relate to epigenetic aging using DNA methylation clocks in a sample of 158 individuals from the Detroit Neighborhood Health Study.

Tractor improves GWAS power and resolution by including admixed individuals through local ancestry-aware analysis.

The paper uses machine learning to identify factors predicting prospective risk of post-traumatic stress symptoms, finding that prior PTSS, loneliness, and a specific DNA methylation site are key predictors.

The paper examines polygenic risk scores for PTSD severity and chronicity in World Trade Center responders, finding significant genetic contributions and associations with brain imaging phenotypes.

This study identifies genetic variants associated with self-reported childhood maltreatment and finds significant genetic correlations with depressive symptoms.

The paper identifies and validates modifiable factors for depression prevention using UK Biobank data and Mendelian randomization.

The paper identifies sex-specific changes in monocyte proportions in males with PTSD using methylomic data, showing no such changes in females.

The paper examines how genetic and environmental factors influence DNA methylation at variably methylated regions in neonatal blood, finding that combined effects best explain methylation variability.

This study examines how polygenic risk and protective factors like unit cohesion and trait resilience affect the risk of depression in US Army soldiers after combat deployment.

This study identifies ten novel methylation loci associated with PTSD through a meta-analysis of 1,896 cases and controls across ten cohorts, highlighting the AHRR locus and its link to kynurenine levels.

The paper identifies SNRNP35 as a trauma type-specific PTSD gene through analysis of genetically regulated gene expression in PTSD cases and controls.

This study uses Mendelian randomization to test causal relationships between physical activity and depression, finding protective effects of objective activity measures but not self-reported ones.

This study uses genetic data to show that educational attainment causally reduces PTSD risk, with economic status mediating this relationship.