Faraone, S. V. et al. Attention-deficit/hyperactivity disorder. Nat. Rev. Dis. Primers 1, 15020 (2015).
Franke, B. et al. Live fast, die young? A review on the developmental trajectories of ADHD across the lifespan. Eur. Neuropsychopharmacol. 28, 1059–1088 (2018).
Fairchild, G. et al. Conduct disorder. Nat. Rev. Dis. Primers 5, 43 (2019).
Canino, G., Polanczyk, G., Bauermeister, J. J., Rohde, L. A. & Frick, P. J. Does the prevalence of CD and ODD vary across cultures? Soc. Psychiatry Psychiatr. Epidemiol. 45, 695–704 (2010).
Nock, M. K., Kazdin, A. E., Hiripi, E. & Kessler, R. C. Lifetime prevalence, correlates, and persistence of oppositional defiant disorder: results from the National Comorbidity Survey Replication. J. Child Psychol. Psychiatry 48, 703–713 (2007).
Dalsgaard, S. et al. Incidence rates and cumulative incidences of the full spectrum of diagnosed mental disorders in childhood and adolescence. JAMA Psychiatry 77, 155–164 (2020).
Scott, J. G. et al. Mortality in individuals with disruptive behavior disorders diagnosed by specialist services—A nationwide cohort study. Psychiatry Res. 251, 255–260 (2017).
Dalsgaard, S., Ostergaard, S. D., Leckman, J. F., Mortensen, P. B. & Pedersen, M. G. Mortality in children, adolescents, and adults with attention deficit hyperactivity disorder: a nationwide cohort study. Lancet 385, 2190–2196 (2015).
Larson, K., Russ, S. A., Kahn, R. S. & Halfon, N. Patterns of comorbidity, functioning, and service use for US children with ADHD, 2007. Pediatrics 127, 462–470 (2011).
Maughan, B., Rowe, R., Messer, J., Goodman, R. & Meltzer, H. Conduct disorder and oppositional defiant disorder in a national sample: developmental epidemiology. J. Child Psychol. Psychiatry 45, 609–621 (2004).
Smalley, S. L. et al. Prevalence and psychiatric comorbidity of attention-deficit/hyperactivity disorder in an adolescent Finnish population. J. Am. Acad. Child Adolesc. Psychiatry 46, 1575–1583 (2007).
Biederman, J. et al. Is ADHD a risk factor for psychoactive substance use disorders? Findings from a four-year prospective follow-up study. J. Am. Acad. Child Adolesc. Psychiatry 36, 21–29 (1997).
Groenman, A. P. et al. Substance use disorders in adolescents with attention deficit hyperactivity disorder: a 4-year follow-up study. Addiction 108, 1503–1511 (2013).
Ottosen, C., Petersen, L., Larsen, J. T. & Dalsgaard, S. Gender differences in associations between attention-deficit/hyperactivity disorder and substance use disorder. J. Am. Acad. Child Adolesc. Psychiatry 55, 227–234 (2016).
Dalsgaard, S., Mortensen, P. B., Frydenberg, M. & Thomsen, P. H. Conduct problems, gender and adult psychiatric outcome of children with attention-deficit hyperactivity disorder. Br. J. Psychiatry 181, 416–421 (2002).
Pingault, J. B. et al. Childhood hyperactivity, physical aggression and criminality: a 19-year prospective population-based study. PLoS ONE 8, e62594 (2013).
Mannuzza, S., Klein, R. G., Konig, P. H. & Giampino, T. L. Hyperactive boys almost grown up. IV. Criminality and its relationship to psychiatric status. Arch. Gen. Psychiatry 46, 1073–1079 (1989).
Dekkers, T. J., Popma, A., Agelink van Rentergem, J. A., Bexkens, A. & Huizenga, H. M. Risky decision making in attention-deficit/hyperactivity disorder: a meta-regression analysis. Clin. Psychol. Rev. 45, 1–16 (2016).
Faraone, S. V. & Larsson, H. Genetics of attention deficit hyperactivity disorder. Mol. Psychiatry 24, 562–575 (2019).
Slutske, W. S. et al. Modeling genetic and environmental influences in the etiology of conduct disorder: a study of 2,682 adult twin pairs. J. Abnorm. Psychol. 106, 266–279 (1997).
Goldstein, R. B., Prescott, C. A. & Kendler, K. S. Genetic and environemental factors in conduct problems and adult antisocial behavior among adult female twins. J. Nerv. Ment. Dis. 189, 201–209 (2001).
Rose, R. J., Dick, D. M., Viken, R. J., Pulkkinen, L. & Kaprio, J. Genetic and environmental effects on conduct disorder and alcohol dependence symptoms and their covariation at age 14. Alcohol. Clin. Exp. Res. 28, 1541–1548 (2004).
Thapar, A., Harrington, R. & McGuffin, P. Examining the comorbidity of ADHD-related behaviours and conduct problems using a twin study design. Br. J. Psychiatry 179, 224–229 (2001).
Christiansen, H. et al. Co-transmission of conduct problems with attention-deficit/hyperactivity disorder: familial evidence for a distinct disorder. J Neural Transm. 115, 163–175 (2008).
Faraone, S. V., Biederman, J., Mennin, D., Russell, R. & Tsuang, M. T. Familial subtypes of attention deficit hyperactivity disorder: a 4-year follow-up study of children from antisocial-ADHD families. J. Child Psychol. Psychiatry 39, 1045–1053 (1998).
Hamshere, M. L. et al. High loading of polygenic risk for ADHD in children with comorbid aggression. Am. J. Psychiatry 170, 909–916 (2013).
Dick, D. M., Viken, R. J., Kaprio, J., Pulkkinen, L. & Rose, R. J. Understanding the covariation among childhood externalizing symptoms: genetic and environmental influences on conduct disorder, attention deficit hyperactivity disorder, and oppositional defiant disorder symptoms. J. Abnorm. Child Psychol. 33, 219–229 (2005).
Martin, N. C., Levy, F., Pieka, J. & Hay, D. A. A Genetic study of attention deficit hyperactivity disorder, conduct disorder, oppositional defiant disorder and reading disability: aetiological overlaps and implications. Int. J. Disabil. Dev. Educ. 53, 21–34 (2006).
Faraone, S. V., Biederman, J., Keenan, K. & Tsuang, M. T. Separation of DSM-III attention deficit disorder and conduct disorder: evidence from a family-genetic study of American child psychiatric patients. Psychol. Med. 21, 109–121 (1991).
Knopik, V. S. et al. DSM-IV defined conduct disorder and oppositional defiant disorder: an investigation of shared liability in female twins. Psychol. Med. 44, 1053–1064 (2014).
Dick, D. M. et al. Genome-wide association study of conduct disorder symptomatology. Mol. Psychiatry 16, 800–808 (2011).
Aebi, M. et al. Gene-set and multivariate genome-wide association analysis of oppositional defiant behavior subtypes in attention-deficit/hyperactivity disorder. Am. J. Med. Genet. Part B 171, 573–588 (2016).
Pappa, I. et al. A genome-wide approach to children’s aggressive behavior: The EAGLE consortium. Am. J. Med. Genet. Part B 171, 562–572 (2016).
Tielbeek, J. J. et al. Genome-wide association studies of a broad spectrum of antisocial behavior. JAMA Psychiatry 74, 1242–1250 (2017).
Anney, R. J. et al. Conduct disorder and ADHD: evaluation of conduct problems as a categorical and quantitative trait in the international multicentre ADHD genetics study. Am. J. Med. Genet. Part B 147B, 1369–1378 (2008).
Brevik, E. J. et al. Genome-wide analyses of aggressiveness in attention-deficit hyperactivity disorder. Am. J. Med. Genet. Part B 171, 733–747 (2016).
Bulik-Sullivan, B. K. et al. LD Score regression distinguishes confounding from polygenicity in genome-wide association studies. Nat. Genet. 47, 291–295 (2015).
Bulik-Sullivan, B. et al. An atlas of genetic correlations across human diseases and traits. Nat. Genet. 47, 1236–1241 (2015).
Zhu, Z. et al. Causal associations between risk factors and common diseases inferred from GWAS summary data. Nat. Commun. 9, 224 (2018).
de Leeuw, C. A., Mooij, J. M., Heskes, T. & Posthuma, D. MAGMA: generalized gene-set analysis of GWAS data. PLoS Comput. Biol. 11, e1004219 (2015).
GTEx Consortium. Human genomics. The Genotype-Tissue Expression (GTEx) pilot analysis: multitissue gene regulation in humans. Science 348, 648–660 (2015).
Barbeira, A. N. et al. Exploring the phenotypic consequences of tissue specific gene expression variation inferred from GWAS summary statistics. Nat. Commun. 9, 1825 (2018).
Shao, J. & Wu, C. F. J. A general theory for Jackknife variance estimation. Ann. Stat. 17, 1176–1197 (1989).
Okbay, A. et al. Genome-wide association study identifies 74 loci associated with educational attainment. Nature 533, 539–542 (2016).
Davies, G. et al. Genome-wide association study of cognitive functions and educational attainment in UK Biobank (N=112 151). Mol. Psychiatry 21, 758–767 (2016).
Sniekers, S. et al. Genome-wide association meta-analysis of 78,308 individuals identifies new loci and genes influencing human intelligence. Nat. Genet. 49, 1107–1112 (2017).
Demontis, D. et al. Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder. Nat. Genet. 51, 63–75 (2019).
Lee, P. H. et al. Genome wide meta-analysis identifies genomic relationships, novel loci, and pleiotropic mechanisms across eight psychiatric disorders. Cell 179, 1469–1482 (2019).
Schizophrenia Working Group of the Psychiatric Genomics. Biological insights from 108 schizophrenia-associated genetic loci. Nature 511, 421–427 (2014).
Ikeda, M. et al. A genome-wide association study identifies two novel susceptibility loci and trans population polygenicity associated with bipolar disorder. Mol. Psychiatry 23, 639–647 (2018).
Ruderfer, D. M. et al. Polygenic dissection of diagnosis and clinical dimensions of bipolar disorder and schizophrenia. Mol. Psychiatry 19, 1017–1024 (2014).
Zhang, S. L. et al. STIM1 is a Ca2+ sensor that activates CRAC channels and migrates from the Ca2+ store to the plasma membrane. Nature 437, 902–905 (2005).
Yen, M. & Lewis, R. S. Numbers count: How STIM and Orai stoichiometry affect store-operated calcium entry. Cell Calcium 79, 35–43 (2019).
Klejman, M. E. et al. Expression of STIM1 in brain and puncta-like co-localization of STIM1 and ORAI1 upon depletion of Ca(2+) store in neurons. Neurochem. Int. 54, 49–55 (2009).
Majewski, L. et al. Overexpression of STIM1 in neurons in mouse brain improves contextual learning and impairs long-term depression. Biochim. Biophys. Acta 1864, 1071–1087 (2017).
Garcia-Alvarez, G. et al. Impaired spatial memory and enhanced long-term potentiation in mice with forebrain-specific ablation of the Stim genes. Front. Behav. Neurosci. 9, 180 (2015).
Ferreira, M. A. et al. Collaborative genome-wide association analysis supports a role for ANK3 and CACNA1C in bipolar disorder. Nat. Genet. 40, 1056–1058 (2008).
Cross-Disorder Group of the Psychiatric Genomics. Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis. Lancet 381, 1371–1379 (2013).
Nanou, E. & Catterall, W. A. Calcium channels, synaptic plasticity, and neuropsychiatric disease. Neuron 98, 466–481 (2018).
Robinson, E. B. et al. Genetic risk for autism spectrum disorders and neuropsychiatric variation in the general population. Nat. Genet. 48, 552–555 (2016).
Bralten, J. et al. Autism spectrum disorders and autistic traits share genetics and biology. Mol. Psychiatry 23, 1205–1212 (2018).
van Beijsterveldt, C. E., Bartels, M., Hudziak, J. J. & Boomsma, D. I. Causes of stability of aggression from early childhood to adolescence: a longitudinal genetic analysis in Dutch twins. Behav. Genet. 33, 591–605 (2003).
Porsch, R. M. et al. Longitudinal heritability of childhood aggression. Am. J. Med. Genet. Part B 171, 697–707 (2016).
Huesmann, L. R., Eron, L. D., Lefkowitz, M. M. & Walder, L. O. Stability of aggression over time and generations. Dev. Psychol. 20, 1120–1134 (1984).
Zoccolillo, M., Pickles, A., Quinton, D. & Rutter, M. The outcome of childhood conduct disorder: implications for defining adult personality disorder and conduct disorder. Psychol. Med. 22, 971–986 (1992).
Erskine, H. E. et al. Long-term outcomes of attention-deficit/hyperactivity disorder and conduct disorder: a systematic review and meta-analysis. J. Am. Acad. Child Adolesc. Psychiatry 55, 841–850 (2016).
Estevez, E., Jimenez, T. I. & Moreno, D. Aggressive behavior in adolescence as a predictor of personal, family, and school adjustment problems. Psicothema 30, 66–73 (2018).
Bierman, K. L. et al. School outcomes of aggressive-disruptive children: prediction from kindergarten risk factors and impact of the fast track prevention program. Aggress. Behav. 39, 114–130 (2013).
Ainsworth, S. E. & Maner, J. K. Sex begets violence: mating motives, social dominance, and physical aggression in men. J. Pers. Soc. Psychol. 103, 819–829 (2012).
Pedersen, C. B. et al. The iPSYCH2012 case-cohort sample: new directions for unravelling genetic and environmental architectures of severe mental disorders. Mol. Psychiatry 23, 6–14 (2018).
Borglum, A. D. et al. Genome-wide study of association and interaction with maternal cytomegalovirus infection suggests new schizophrenia loci. Mol. Psychiatry 19, 325–333 (2014).
Hollegaard, M. V. et al. Robustness of genome-wide scanning using archived dried blood spot samples as a DNA source. BMC Genet. 12, 58 (2011).
Mors, O., Perto, G. P. & Mortensen, P. B. The Danish Psychiatric Central Research Register. Scand. J. Public Health 39, 54–57 (2011).
Demontis, D. et al. Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder. Nat. Genet. 51, 63–75 (2018).
Lam, M. et al. RICOPILI: Rapid Imputation for COnsortias PIpeLIne. Bioinformatics https://doi.org/10.1093/bioinformatics/btz633 (2019).
Delaneau, O., Marchini, J. & Zagury, J. F. A linear complexity phasing method for thousands of genomes. Nat. Methods 9, 179–181 (2011).
Howie, B., Marchini, J. & Stephens, M. Genotype imputation with thousands of genomes. G3 1, 457–470 (2011).
1000 Genomes Project Consortium. An integrated map of genetic variation from 1092 human genomes. Nature 491, 56–65 (2012).
Price, A. L. et al. Long-range LD can confound genome scans in admixed populations. Am. J. Hum. Genet. 83, 132–135 (2008).
Purcell, S. et al. PLINK: a tool set for whole-genome association and population-based linkage analyses. Am. J. Hum. Genet. 81, 559–575 (2007).
Chang, C. C. et al. Second-generation PLINK: rising to the challenge of larger and richer datasets. Gigascience 4, 7 (2015).
Price, A. L. et al. Principal components analysis corrects for stratification in genome-wide association studies. Nat. Genet. 38, 904–909 (2006).
Galinsky, K. J. et al. Fast principal-component analysis reveals convergent evolution of ADH1B in Europe and East Asia. Am. J. Hum. Genet. 98, 456–472 (2016).
Willer, C. J., Li, Y. & Abecasis, G. R. METAL: fast and efficient meta-analysis of genomewide association scans. Bioinformatics 26, 2190–2191 (2010).
Yang, J., Lee, S. H., Goddard, M. E. & Visscher, P. M. GCTA: a tool for genome-wide complex trait analysis. Am. J. Hum. Genet. 88, 76–−82 (2011).
GTEx Consortium. The Genotype-Tissue Expression (GTEx) project. Nat. Genet. 45, 580–585 (2013).
Gamazon, E. R. et al. A gene-based association method for mapping traits using reference transcriptome data. Nat. Genet. 47, 1091–1098 (2015).
The 1000 Genomes Project Consortium. A global reference for human genetic variation. Nature 526, 68–74 (2015).
Hubel, C. et al. Genomics of body fat percentage may contribute to sex bias in anorexia nervosa. Am. J. Med. Genet. Part B 180, 428–438 (2019).
Lee, S. H., Goddard, M. E., Wray, N. R. & Visscher, P. M. A better coefficient of determination for genetic profile analysis. Genet. Epidemiol. 36, 214–224 (2012).