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Uncovering the genetic architecture of broad antisocial behavior through a genome-wide association study meta-analysis
   

Uncovering the genetic architecture of broad antisocial behavior through a genome-wide association study meta-analysis

Jorim J Tielbeek, Emil Uffelmann, Benjamin S Williams, Lucía Colodro-Conde, Éloi Gagnon, Travis T Mallard, Brandt E Levitt, Philip R Jansen, Ada Johansson, Hannah M Sallis, …
Molecular psychiatry, Vol.27(11), pp.4453-4463
01/11/2022
:
https://hdl.handle.net/10523/43947
 
Aggression - psychology Antisocial Personality Disorder - genetics Conduct Disorder - genetics Conduct Disorder - psychology Genome-Wide Association Study Membrane Proteins - genetics Multifactorial Inheritance - genetics Nerve Tissue Proteins - genetics neuroscience
Despite the substantial heritability of antisocial behavior (ASB), specific genetic variants robustly associated with the trait have not been identified. The present study by the Broad Antisocial Behavior Consortium (BroadABC) meta-analyzed data from 28 discovery samples (N = 85,359) and five independent replication samples (N = 8058) with genotypic data and broad measures of ASB. We identified the first significant genetic associations with broad ASB, involving common intronic variants in the forkhead box protein P2 (FOXP2) gene (lead SNP rs12536335, p = 6.32 × 10 ). Furthermore, we observed intronic variation in Foxp2 and one of its targets (Cntnap2) distinguishing a mouse model of pathological aggression (BALB/cJ strain) from controls (BALB/cByJ strain). Polygenic risk score (PRS) analyses in independent samples revealed that the genetic risk for ASB was associated with several antisocial outcomes across the lifespan, including diagnosis of conduct disorder, official criminal convictions, and trajectories of antisocial development. We found substantial genetic correlations of ASB with mental health (depression r  = 0.63, insomnia r  = 0.47), physical health (overweight r  = 0.19, waist-to-hip ratio r  = 0.32), smoking (r  = 0.54), cognitive ability (intelligence r  = -0.40), educational attainment (years of schooling r  = -0.46) and reproductive traits (age at first birth r  = -0.58, father's age at death r  = -0.54). Our findings provide a starting point toward identifying critical biosocial risk mechanisms for the development of ASB.

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url
https://rdcu.be/d23jo
Published (Version of record)Free to read via Springer Nature SharedIt Initiative
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