Erin C. Dunn

The paper shows that differences in adolescent cortical maturation patterns predict psychiatric symptoms, with early maturing sensory regions linked to symptoms four years before their onset.

The paper examines how prenatal social disadvantage and psychosocial stress affect DNA methylation in children and their potential role in psychopathology.

The paper identifies age-dependent methylation quantitative trait loci (longitudinal mQTLs) across the lifespan using blood DNAm data from two cohorts, finding consistent genotype-by-age effects and associations with multiple phenotypes.

The paper investigates how childhood adversity during sensitive periods affects DNA methylation in genes regulating developmental plasticity using a gene set-based approach.

The paper examines the relationship between methylation age and brain age in adolescents, finding they are largely independent and influenced by different factors like smoking and BMI.

This study shows that changes in socioeconomic environment during childhood affect DNA methylation at age 7, with middle childhood being a sensitive period for socioeconomic adversity's impact.

This paper conducts a multi-ancestry GWAS of major depression, identifying 190 loci and 354 genes, with findings showing increased fine-mapping power and bidirectional BMI relationship in European ancestry samples.

The paper assesses how changes in data versions and analytic methods affect the reproducibility of epigenome-wide association study results using the ALSPAC cohort.

This review examines the association between socioeconomic position (SEP) and DNA methylation across the life course, finding that early-life SEP and persistent low SEP strongly influence DNAm patterns.

The paper examines how genetic pathways regulating sensitive periods and socioeconomic disadvantage interact to influence depression risk using genome-wide data and developmental gene expression patterns.

This study maps DNA methylation changes across the human life course using data from 7,037 individuals, showing increased variability and age-related mean changes at specific CpG sites.

This study examines how time-varying childhood adversity affects DNA methylation across development, finding persistent effects at age 15 and resolving differences by adolescence.

The paper examines how genetic risk scores for depression relate to different patterns of depressive symptoms from childhood to adolescence.

This study identifies traits associated with polygenic risk for depression using UK Biobank data and finds causal links between depression risk and brain structure, as well as environmental interactions.

This study identifies 73 genome-wide significant loci for mood disorders, revealing shared and distinct genetic factors between major depressive disorder and bipolar disorder.

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

This study investigates whether genetic variation in the Major Histocompatibility Complex (MHC) is associated with depression risk, finding no significant associations at a conservative threshold.

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 investigates the genetic and environmental links between major depressive disorder and traumatic experiences using UK Biobank data, finding shared genetic factors and distinct patterns in trauma-exposed individuals.

This study identifies 40 CpG sites with differential methylation at age 7 linked to adversity exposure timing, showing infancy as a sensitive period for DNAm changes.

The paper applies polygenic risk scoring to a large family with bipolar and depressive disorders to study genetic risk patterns and anticipation.

The paper examines how childhood adversity exposure affects epigenetic aging using DNA methylation clocks in children, finding that timing and type of adversity exposure significantly influence biological age.

Genome-wide association meta-analysis of 130,664 major depression cases and 330,470 controls identifies 44 independent risk loci enriched in cortical neurons, conserved mammalian regions, splicing networks, and antidepressant targets.