School of Criminology,University of Montreal and The Montreal Mental Health University Institute,Canada.
Centre-affiliated Researcher,Child Psychopathology Unit,Scientific Institute, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Eugenio Medea,Italy.
Br J Psychiatry. 2019 Mar;214(3):137-145. doi: 10.1192/bjp.2018.251.
Heritability of antisocial behaviour is estimated at approximately 50% and involves multiple genes.AimsTo investigate the cumulative genetic effects of 116 single nucleotide polymorphisms mapping to 11 candidate serotonergic genes and antisocial behaviours, in adolescence and in early adulthood.
Participants were 410 male members of the Quebec Longitudinal Study of Kindergarten Children, a population-based cohort followed up prospectively from age 6 to age 23. The serotonergic genes were selected based on known physiological processes and prior associations with antisocial behaviours. Antisocial behaviours were self-reported and assessed by using semi-structured interviews in adolescence and in adulthood.
Cumulative, haplotype-based contributions of serotonergic genes conferring risk and protection for antisocial behaviours were detected by using multilocus genetic profile risk scores (MGPRSs) and multilocus genetic profile protection scores (MGPPSs). Cumulatively, haplotype-based MGPRSs and MGPPSs contributed to 9.6, 8.5 and 15.2% of the variance in general delinquency in adolescence, property/violent crimes in early adulthood and physical partner violence in early adulthood, respectively.
This study extends previous research by showing a cumulative effect of multiple haplotypes conferring risk and protection to antisocial behaviours in adolescence and early adulthood. The findings further support the relevance of concomitantly considering multiple serotonergic polymorphisms to better understand the genetic aetiology of antisocial behaviours. Future studies should investigate the interplay between risk and protective haplotype-based multilocus genetic profile scores with the environment.
I.O.-M. holds a Canada Research Chair in the developmental origins of vulnerability and resilience.
反社会行为的遗传率约为 50%，涉及多个基因。
研究 116 个单核苷酸多态性映射到 11 个候选 5-羟色胺能基因与青少年和成年早期反社会行为的累积遗传效应。
参与者为魁北克纵向幼儿园儿童研究的 410 名男性成员，这是一个基于人群的队列，从 6 岁到 23 岁进行前瞻性随访。选择 5-羟色胺能基因是基于已知的生理过程和先前与反社会行为的关联。反社会行为通过青少年和成年期的半结构化访谈进行自我报告和评估。
通过多基因遗传谱风险评分（MGPRSs）和多基因遗传谱保护评分（MGPPSs）检测到与反社会行为相关的风险和保护的累积、基于单倍型的 5-羟色胺能基因贡献。累积的、基于单倍型的 MGPRSs 和 MGPPSs 分别解释了青少年期一般犯罪、成年早期财产/暴力犯罪和成年早期身体伴侣暴力的 9.6%、8.5%和 15.2%的变异。
这项研究通过显示多个单倍型的累积效应，为青少年和成年早期的反社会行为提供了风险和保护，扩展了先前的研究。研究结果进一步支持同时考虑多个 5-羟色胺能多态性来更好地理解反社会行为的遗传病因的相关性。未来的研究应该研究风险和保护的基于单倍型的多基因遗传谱评分与环境之间的相互作用。
I.O.-M. 拥有加拿大发育起源脆弱性和恢复力研究主席。
