Miguel Casas

This paper develops multi-polygenic scores to predict externalizing behavior in children, finding that combining multiple PGSs increases variance explained and that socioeconomic status moderates this effect.

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 genetic risk loci and factors underlying clinical subtypes of bipolar disorder using GWAS and meta-analysis.

This study identifies 30 genome-wide significant loci for obsessive-compulsive disorder (OCD) using a large GWAS, linking risk to specific brain cell types and shared genetic risk with other psychiatric and non-psychiatric traits.

Meta-analysis of 41,917 European-ancestry bipolar disorder cases versus 371,549 controls yields 64 risk loci (33 novel), neuronal and synaptic gene enrichment, and 15 eQTL-prioritized genes.

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

The paper examines common genetic variants' contribution to bipolar disorder risk in multiplex families and finds higher polygenic risk scores in affected individuals compared to controls and unaffected family members.

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

This study identifies 30 genome-wide significant loci associated with bipolar disorder, including novel genes involved in ion channels, neurotransmitters, and synaptic components.

This study identifies 114 genome-wide significant loci for schizophrenia and bipolar disorder, with specific subphenotype associations and four genes distinguishing the disorders.

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.