Esther Walton

This study integrates prenatal exposures and genetics to predict DNA methylation at birth, finding that the exposome explains additional variation beyond genetic factors.

Across 15 cohorts (birth to 24 years), 20 epigenetic clocks and eight brain age models predicted chronological age modestly, stabilizing by middle childhood; their age residuals were weakly associated.

This study identifies altered structure-function coupling in bipolar disorder and links these changes to genetic loci involved in neuronal development and signaling.

This study uses longitudinal meta-regression to examine how DNA methylation effects on child health outcomes vary by timing, finding larger effects in childhood but noisier associations and time-specific signals.

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.

The paper estimates the variance explained by DNA methylation at birth for childhood phenotypes using GREML, finding moderate to large contributions for gestational age and birth weight but near-zero for BMI, IQ, and ADHD symptoms.

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 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.

This study uses Mendelian randomization to examine bidirectional causal effects between brain morphology and Alzheimer's disease risk across different life stages.

The paper outlines the protocol for the EarlyCause project, which investigates the biological mechanisms linking early-life stress to psycho-cardio-metabolic multi-morbidity using longitudinal data, animal models, and cellular systems.

The paper analyzes DNA methylation changes across birth to late adolescence in two cohorts, finding widespread nonlinear changes and sex-specific patterns.

This study identifies DNA methylation sites at birth associated with ADHD symptoms later in childhood, but finds no such associations at school age.

The paper develops deep learning models to assess the quality of subcortical brain shape models from MRI, reducing human rater time by 46-70%.

This study evaluates the causal relationship between DNA methylation and CRP using Mendelian randomization and finds potential causal effects of DNA methylation on CRP levels at three CpG sites.

The paper identifies 25 genetic loci associated with subcortical brain structure volumes in over 40,000 individuals, revealing novel biology and potential drug targets.