Philip J. Asherson

The paper benchmarks and optimizes a normative modeling framework for brain morphometry across the lifespan using MFPR, showing excellent accuracy and stability.

This study analyzes structural brain asymmetries in ADHD using 39 datasets, finding small effects that do not meet study-wide significance thresholds.

The paper analyzes cortical thickness trajectories in 17,075 individuals to show peak thickness in childhood, steep decline in early adulthood, and slower decline later, with notable exceptions and significant inter-individual variability.

This study uses machine learning to show that structural brain anomalies in ADHD are similar in children and adults, supporting continuity of the disorder's pathophysiology.

The paper analyzes sex differences in brain structure variability across the lifespan using a large dataset, finding greater male variability in subcortical volumes, cortical surface area, and thickness in most regions.

This study analyzes subcortical volume changes across the lifespan using MRI data from 18,605 individuals, finding age-related declines in some structures and increases in others.

This study identifies nine new genetic loci associated with ADHD and shows shared genetic architecture between childhood and adult ADHD.

The paper investigates how genetic variation in DRD4 interacts with seasonal daylight changes to influence inattention, finding support for the Spring-focus hypothesis and seasonal patterns in ADHD-related symptoms.

Genome-wide association meta-analysis of 20,183 ADHD cases and 35,191 controls finds 12 significant loci; signal concentrates in conserved regions, constrained genes, and CNS regulatory elements.

The paper examines functional connectivity differences in adolescents and adults with persistent and remitted ADHD compared to controls using EEG and graph-theory metrics.

This study investigates genetic mechanisms underlying sex bias in ADHD prevalence using genome-wide data and finds no mean polygenic burden difference across sexes but increased risk in female siblings and comorbid conditions.