Bru Cormand

This study identifies shared genetic architecture between schizophrenia and substance use disorders using GWAS and genomic methods, finding significant genetic correlations and bidirectional causal relationships.

The paper identifies cell-type-specific DNA methylation patterns in excitatory neurons associated with suicide using postmortem brain tissue.

The paper identifies sex-specific miRNA signatures in the medial prefrontal cortex associated with cannabinoid addiction-like behavior in female mice.

This study investigates genotype-phenotype correlations in SYNGAP1 Encephalopathy, finding that variant location and type, along with modifier genes, influence clinical severity and autistic traits.

This study shows that rbfox1 loss of function in zebrafish disrupts stress-related gene expression and increases cortisol levels during development, leading to behavioral and physiological signs of allostatic overload in adulthood.

This study identifies 80 genome-wide significant associations for endometriosis and adenomyosis in 1.4 million women, uncovering novel loci and pathways involved in disease mechanisms.

This study investigates SUD heterogeneity by analyzing polygenic scores for psychiatric traits and their interactions with environmental factors in a deeply phenotyped SUD cohort.

This study identifies pleiotropic effects of dopaminergic and serotonergic genes on addiction, aggression, and related behaviors through GWAS and TWAS analyses across multiple datasets.

This study investigates the behavioral effects of rbfox1 deficiency in zebrafish, finding multiple behavioral changes that resemble those in Rbfox1-deficient mice and psychiatric patients.

This study shows that ywhaz gene deficiency in zebrafish affects brain activity and behavior, with altered neuronal connectivity and monoamine levels.

This study investigates the genetic contribution of dopaminergic and serotonergic pathways to eight psychiatric disorders using GWAS data from the Psychiatric Genomics Consortium.

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

This study identifies dopaminergic signaling as a genetic link between ADHD and obesity through genome-wide analyses and brain volume associations.

This study identifies risk variants and characterizes the polygenic architecture of ADHD comorbid with disruptive behavior disorders through a large GWAS meta-analysis.

This study identifies three novel genes associated with ADHD by linking genetic variants to differential DNA methylation and gene expression in brain tissues.

The paper investigates the role of inherited and de novo truncating mutations in high functioning autism and identifies pleiotropic effects of LRP1 variants across psychiatric phenotypes.

This paper conducts a genome-wide association study of cocaine dependence, finding shared genetic risk factors with comorbid psychiatric conditions.

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.

This study shows common genetic variants significantly contribute to migraine family clustering, with higher burden in familial cases compared to population-based cases.

This study identifies rare paternally-inherited structural variants contributing to autism by disrupting noncoding regions and coding genes, with differential parental contributions.

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.