Henrik Larsson

This study identifies 52 genetic variants associated with adolescent-onset depression through a large GWAS, revealing age-specific mechanisms and potential drug targets.

This study uses genome-wide meta-regression to analyze social behavior across different contexts, ages, and reporters, identifying six genetic loci and showing modest heritability.

This study identifies 80 medical conditions associated with ADHD genetic liability in adults without ADHD diagnosis using EHR data.

This paper conducts a GWAS of subclinical obsessive-compulsive symptoms (OCS) in 33,943 individuals, finding polygenic risk and genetic overlap with OCD.

The paper maps genetic and environmental influences on autistic traits across Sweden and the UK using twin study data, revealing geographical variations in their aetiology.

This study conducts a genome-wide association meta-analysis of childhood aggression across multiple raters, instruments, and ages, identifying genetic correlations with various traits but no genome-wide significant SNPs.

This study finds ADHD is genetically more closely linked to neurodevelopmental disorders than externalizing or internalizing disorders after accounting for a general psychopathology factor.

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

This study uses Swedish registry data to predict substance use disorders in ADHD youth with machine learning models, achieving moderate accuracy even without prior SUD diagnosis.

This study investigates the association between rare copy number variants (CNVs) and neurodevelopmental problems (NPs) in children, finding sex-specific effects in anxiety/depression.

This study evaluates ADHD genetic risk variants' association with general psychopathology and specific neurodevelopmental traits, finding general pleiotropy and a specific link to hyperactivity/impulsivity.

The paper finds genetic correlations between psychiatric disorders and related continuous traits in a Swedish twin sample, suggesting disorders are extreme ends of continuous traits.

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.