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4. Genome-wide Association Meta-analysis of Childhood and Adolescent Internalizing Symptoms

Author

Jami, Eshim S, Hammerschlag, Anke R, Ip, Hill F, Allegrini, Andrea G, Benyamin, Beben, Border, Richard, Diemer, Elizabeth W, Jiang, Chang, Karhunen, Ville, Lu, Yi, Lu, Qing, Mallard, Travis T, Mishra, Pashupati P, Nolte, Ilja M, Palviainen, Teemu, Peterson, Roseann E, Sallis, Hannah M, Shabalin, Andrey A, Tate, Ashley E, Thiering, Elisabeth, Vilor-Tejedor, Natàlia, Wang, Carol, Zhou, Ang, Adkins, Daniel E, Alemany, Silvia, Ask, Helga, Chen, Qi, Corley, Robin P, Ehli, Erik A, Evans, Luke M, Havdahl, Alexandra, Hagenbeek, Fiona A, Hakulinen, Christian, Henders, Anjali K, Hottenga, Jouke Jan, Korhonen, Tellervo, Mamun, Abdullah, Marrington, Shelby, Neumann, Alexander, Rimfeld, Kaili, Rivadeneira, Fernando, Silberg, Judy L, van Beijsterveldt, Catharina E, Vuoksimaa, Eero, Whipp, Alyce M, Tong, Xiaoran, Andreassen, Ole A, Boomsma, Dorret I, Brown, Sandra A, Burt, S Alexandra, Copeland, William, Dick, Danielle M, Harden, K Paige, Harris, Kathleen Mullan, Hartman, Catharina A, Heinrich, Joachim, Hewitt, John K, Hopfer, Christian, Hypponen, Elina, Jarvelin, Marjo-Riitta, Kaprio, Jaakko, Keltikangas-Järvinen, Liisa, Klump, Kelly L, Krauter, Kenneth, Kuja-Halkola, Ralf, Larsson, Henrik, Lehtimäki, Terho, Lichtenstein, Paul, Lundström, Sebastian, Maes, Hermine H, Magnus, Per, Munafò, Marcus R, Najman, Jake M, Njølstad, Pål R, Oldehinkel, Albertine J, Pennell, Craig E, Plomin, Robert, Reichborn-Kjennerud, Ted, Reynolds, Chandra, Rose, Richard J, Smolen, Andrew, Snieder, Harold, Stallings, Michael, Standl, Marie, Sunyer, Jordi, Tiemeier, Henning, Wadsworth, Sally J, Wall, Tamara L, Whitehouse, Andrew JO, Williams, Gail M, Ystrøm, Eivind, Nivard, Michel G, Bartels, Meike, and Middeldorp, Christel M

Subjects
Biological Psychology, Psychology, Serious Mental Illness, Brain Disorders, Pediatric, Human Genome, Genetics, Behavioral and Social Science, Depression, Mental Health, Mental Illness, 2.1 Biological and endogenous factors, 2.3 Psychological, social and economic factors, Mental health, Adolescent, Adult, Aggression, Anxiety, Attention Deficit Disorder with Hyperactivity, Autistic Disorder, Bipolar Disorder, Child, Child, Preschool, Genome-Wide Association Study, Humans, Loneliness, Polymorphism, Single Nucleotide, Schizophrenia, Sleep Initiation and Maintenance Disorders, depression, anxiety, repeated measures, genetic epidemiology, molecular genetics, Medical and Health Sciences, Psychology and Cognitive Sciences, Developmental & Child Psychology, Clinical sciences, Paediatrics, Applied and developmental psychology
Abstract

ObjectiveTo investigate the genetic architecture of internalizing symptoms in childhood and adolescence.MethodIn 22 cohorts, multiple univariate genome-wide association studies (GWASs) were performed using repeated assessments of internalizing symptoms, in a total of 64,561 children and adolescents between 3 and 18 years of age. Results were aggregated in meta-analyses that accounted for sample overlap, first using all available data, and then using subsets of measurements grouped by rater, age, and instrument.ResultsThe meta-analysis of overall internalizing symptoms (INToverall) detected no genome-wide significant hits and showed low single nucleotide polymorphism (SNP) heritability (1.66%, 95% CI = 0.84-2.48%, neffective = 132,260). Stratified analyses indicated rater-based heterogeneity in genetic effects, with self-reported internalizing symptoms showing the highest heritability (5.63%, 95% CI = 3.08%-8.18%). The contribution of additive genetic effects on internalizing symptoms appeared to be stable over age, with overlapping estimates of SNP heritability from early childhood to adolescence. Genetic correlations were observed with adult anxiety, depression, and the well-being spectrum (|rg| > 0.70), as well as with insomnia, loneliness, attention-deficit/hyperactivity disorder, autism, and childhood aggression (range |rg| = 0.42-0.60), whereas there were no robust associations with schizophrenia, bipolar disorder, obsessive-compulsive disorder, or anorexia nervosa.ConclusionGenetic correlations indicate that childhood and adolescent internalizing symptoms share substantial genetic vulnerabilities with adult internalizing disorders and other childhood psychiatric traits, which could partially explain both the persistence of internalizing symptoms over time and the high comorbidity among childhood psychiatric traits. Reducing phenotypic heterogeneity in childhood samples will be key in paving the way to future GWAS success.

Published
2022

5. Genome-wide association study of school grades identifies genetic overlap between language ability, psychopathology and creativity

Author

Rajagopal, Veera M., Ganna, Andrea, Coleman, Jonathan R. I., Allegrini, Andrea, Voloudakis, Georgios, Grove, Jakob, Als, Thomas D., Horsdal, Henriette T., Petersen, Liselotte, Appadurai, Vivek, Schork, Andrew, Buil, Alfonso, Bulik, Cynthia M., Bybjerg-Grauholm, Jonas, Bækvad-Hansen, Marie, Hougaard, David M., Mors, Ole, Nordentoft, Merete, Werge, Thomas, Mortensen, Preben Bo, Breen, Gerome, Roussos, Panos, Plomin, Robert, Agerbo, Esben, Børglum, Anders D., and Demontis, Ditte

Published
2023
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8. Within-sibship genome-wide association analyses decrease bias in estimates of direct genetic effects

Author

Howe, Laurence J, Nivard, Michel G, Morris, Tim T, Hansen, Ailin F, Rasheed, Humaira, Cho, Yoonsu, Chittoor, Geetha, Ahlskog, Rafael, Lind, Penelope A, Palviainen, Teemu, van der Zee, Matthijs D, Cheesman, Rosa, Mangino, Massimo, Wang, Yunzhang, Li, Shuai, Klaric, Lucija, Ratliff, Scott M, Bielak, Lawrence F, Nygaard, Marianne, Giannelis, Alexandros, Willoughby, Emily A, Reynolds, Chandra A, Balbona, Jared V, Andreassen, Ole A, Ask, Helga, Baras, Aris, Bauer, Christopher R, Boomsma, Dorret I, Campbell, Archie, Campbell, Harry, Chen, Zhengming, Christofidou, Paraskevi, Corfield, Elizabeth, Dahm, Christina C, Dokuru, Deepika R, Evans, Luke M, de Geus, Eco JC, Giddaluru, Sudheer, Gordon, Scott D, Harden, K Paige, Hill, W David, Hughes, Amanda, Kerr, Shona M, Kim, Yongkang, Kweon, Hyeokmoon, Latvala, Antti, Lawlor, Deborah A, Li, Liming, Lin, Kuang, Magnus, Per, Magnusson, Patrik KE, Mallard, Travis T, Martikainen, Pekka, Mills, Melinda C, Njølstad, Pål Rasmus, Overton, John D, Pedersen, Nancy L, Porteous, David J, Reid, Jeffrey, Silventoinen, Karri, Southey, Melissa C, Stoltenberg, Camilla, Tucker-Drob, Elliot M, Wright, Margaret J, Hewitt, John K, Keller, Matthew C, Stallings, Michael C, Lee, James J, Christensen, Kaare, Kardia, Sharon LR, Peyser, Patricia A, Smith, Jennifer A, Wilson, James F, Hopper, John L, Hägg, Sara, Spector, Tim D, Pingault, Jean-Baptiste, Plomin, Robert, Havdahl, Alexandra, Bartels, Meike, Martin, Nicholas G, Oskarsson, Sven, Justice, Anne E, Millwood, Iona Y, Hveem, Kristian, Naess, Øyvind, Willer, Cristen J, Åsvold, Bjørn Olav, Koellinger, Philipp D, Kaprio, Jaakko, Medland, Sarah E, Walters, Robin G, Benjamin, Daniel J, Turley, Patrick, Evans, David M, Davey Smith, George, Hayward, Caroline, Brumpton, Ben, Hemani, Gibran, and Davies, Neil M

Subjects
Human Genome, Genetics, Pediatric, 2.1 Biological and endogenous factors, Aetiology, Mental health, Generic health relevance, Genome-Wide Association Study, Humans, Mendelian Randomization Analysis, Multifactorial Inheritance, Phenotype, Polymorphism, Single Nucleotide, Social Science Genetic Association Consortium, Within Family Consortium, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Estimates from genome-wide association studies (GWAS) of unrelated individuals capture effects of inherited variation (direct effects), demography (population stratification, assortative mating) and relatives (indirect genetic effects). Family-based GWAS designs can control for demographic and indirect genetic effects, but large-scale family datasets have been lacking. We combined data from 178,086 siblings from 19 cohorts to generate population (between-family) and within-sibship (within-family) GWAS estimates for 25 phenotypes. Within-sibship GWAS estimates were smaller than population estimates for height, educational attainment, age at first birth, number of children, cognitive ability, depressive symptoms and smoking. Some differences were observed in downstream SNP heritability, genetic correlations and Mendelian randomization analyses. For example, the within-sibship genetic correlation between educational attainment and body mass index attenuated towards zero. In contrast, analyses of most molecular phenotypes (for example, low-density lipoprotein-cholesterol) were generally consistent. We also found within-sibship evidence of polygenic adaptation on taller height. Here, we illustrate the importance of family-based GWAS data for phenotypes influenced by demographic and indirect genetic effects.

Published
2022

10. Genome-Wide Analyses of Vocabulary Size in Infancy and Toddlerhood: Associations With Attention-Deficit/Hyperactivity Disorder, Literacy, and Cognition-Related Traits

Author

Andreassen, Ole A., Bartels, Meike, Boomsma, Dorret, Dale, Philip S., Ehli, Erik, Fernandez-Orth, Dietmar, Guxens, Mònica, Hakulinen, Christian, Harris, Kathleen Mullan, Haworth, Simon, de Hoyos, Lucía, Jaddoe, Vincent, Keltikangas-Järvinen, Liisa, Lehtimäki, Terho, Middeldorp, Christel, Min, Josine L., Mishra, Pashupati P., Njølstad, Pål Rasmus, Sunyer, Jordi, Tate, Ashley E., Timpson, Nicholas, van der Laan, Camiel, Vrijheid, Martine, Vuoksimaa, Eero, Whipp, Alyce, Ystrom, Eivind, ACTION Consortium, Barwon Infant Study investigator group, Verhoef, Ellen, Allegrini, Andrea G., Jansen, Philip R., Lange, Katherine, Wang, Carol A., Morgan, Angela T., Ahluwalia, Tarunveer S., Symeonides, Christos, Eising, Else, Franken, Marie-Christine, Hypponen, Elina, Mansell, Toby, Olislagers, Mitchell, Omerovic, Emina, Rimfeld, Kaili, Schlag, Fenja, Selzam, Saskia, Shapland, Chin Yang, Tiemeier, Henning, Whitehouse, Andrew J.O., Saffery, Richard, Bønnelykke, Klaus, Reilly, Sheena, Pennell, Craig E., Wake, Melissa, Cecil, Charlotte A.M., Plomin, Robert, Fisher, Simon E., and St. Pourcain, Beate

Published
2024
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12. Complement genes contribute sex-biased vulnerability in diverse disorders

Author

Arranz, Maria J, Bakker, Steven, Bender, Stephan, Bramon, Elvira, Collier, David A, Crespo-Facorro, Benedicto, Hall, Jeremy, Iyegbe, Conrad, Jablensky, Assen V, Kahn, René S, Kalaydjieva, Luba, Lawrie, Stephen, Lewis, Cathryn M, Lin, Kuang, Linszen, Don H, Mata, Ignacio, McIntosh, Andrew M, Murray, Robin M, Ophoff, Roel A, Van Os, Jim, Powell, John, Rujescu, Dan, Walshe, Muriel, Weisbrod, Matthias, Wiersma, Durk, Donnelly, Peter, Barroso, Ines, Blackwell, Jenefer M, Brown, Matthew A, Casas, Juan P, Corvin, Aiden, Deloukas, Panos, Duncanson, Audrey, Jankowski, Janusz, Markus, Hugh S, Mathew, Christopher G, Palmer, Colin NA, Plomin, Robert, Rautanen, Anna, Sawcer, Stephen J, Trembath, Richard C, Viswanathan, Ananth C, Wood, Nicholas W, Spencer, Chris CA, Band, Gavin, Bellenguez, Céline, Freeman, Colin, Giannoulatou, Eleni, Hellenthal, Garrett, Pearson, Richard, Pirinen, Matti, Strange, Amy, Su, Zhan, Vukcevic, Damjan, Langford, Cordelia, Blackburn, Hannah, Bumpstead, Suzannah J, Dronov, Serge, Edkins, Sarah, Gillman, Matthew, Gray, Emma, Gwilliam, Rhian, Hammond, Naomi, Hunt, Sarah E, Jayakumar, Alagurevathi, Liddle, Jennifer, McCann, Owen T, Potter, Simon C, Ravindrarajah, Radhi, Ricketts, Michelle, Tashakkori-Ghanbaria, Avazeh, Waller, Matthew, Weston, Paul, Whittaker, Pamela, Widaa, Sara, and McCarthy, Mark I

Subjects
Autoimmune Disease, Schizophrenia, Mental Health, Lupus, Genetics, Brain Disorders, Biotechnology, Aetiology, 2.1 Biological and endogenous factors, Inflammatory and immune system, Adult, Alleles, Complement C3, Complement C4, Female, Genetic Predisposition to Disease, HLA Antigens, Haplotypes, Humans, Lupus Erythematosus, Systemic, Major Histocompatibility Complex, Male, Middle Aged, Sex Characteristics, Sjogren's Syndrome, Young Adult, Schizophrenia Working Group of the Psychiatric Genomics Consortium, General Science & Technology
Abstract

Many common illnesses, for reasons that have not been identified, differentially affect men and women. For instance, the autoimmune diseases systemic lupus erythematosus (SLE) and Sjögren's syndrome affect nine times more women than men1, whereas schizophrenia affects men with greater frequency and severity relative to women2. All three illnesses have their strongest common genetic associations in the major histocompatibility complex (MHC) locus, an association that in SLE and Sjögren's syndrome has long been thought to arise from alleles of the human leukocyte antigen (HLA) genes at that locus3-6. Here we show that variation of the complement component 4 (C4) genes C4A and C4B, which are also at the MHC locus and have been linked to increased risk for schizophrenia7, generates 7-fold variation in risk for SLE and 16-fold variation in risk for Sjögren's syndrome among individuals with common C4 genotypes, with C4A protecting more strongly than C4B in both illnesses. The same alleles that increase risk for schizophrenia greatly reduce risk for SLE and Sjögren's syndrome. In all three illnesses, C4 alleles act more strongly in men than in women: common combinations of C4A and C4B generated 14-fold variation in risk for SLE, 31-fold variation in risk for Sjögren's syndrome, and 1.7-fold variation in schizophrenia risk among men (versus 6-fold, 15-fold and 1.26-fold variation in risk among women, respectively). At a protein level, both C4 and its effector C3 were present at higher levels in cerebrospinal fluid and plasma8,9 in men than in women among adults aged between 20 and 50 years, corresponding to the ages of differential disease vulnerability. Sex differences in complement protein levels may help to explain the more potent effects of C4 alleles in men, women's greater risk of SLE and Sjögren's syndrome and men's greater vulnerability to schizophrenia. These results implicate the complement system as a source of sexual dimorphism in vulnerability to diverse illnesses.

Published
2020

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

Author

Tielbeek, Jorim J., Uffelmann, Emil, Williams, Benjamin S., Colodro-Conde, Lucía, Gagnon, Éloi, Mallard, Travis T., Levitt, Brandt E., Jansen, Philip R., Johansson, Ada, Sallis, Hannah M., Pistis, Giorgio, Saunders, Gretchen R. B., Allegrini, Andrea G., Rimfeld, Kaili, Konte, Bettina, Klein, Marieke, Hartmann, Annette M., Salvatore, Jessica E., Nolte, Ilja M., Demontis, Ditte, Malmberg, Anni L. K., Burt, S. Alexandra, Savage, Jeanne E., Sugden, Karen, Poulton, Richie, Harris, Kathleen Mullan, Vrieze, Scott, McGue, Matt, Iacono, William G., Mota, Nina Roth, Mill, Jonathan, Viana, Joana F., Mitchell, Brittany L., Morosoli, Jose J., Andlauer, Till F. M., Ouellet-Morin, Isabelle, Tremblay, Richard E., Côté, Sylvana M., Gouin, Jean-Philippe, Brendgen, Mara R., Dionne, Ginette, Vitaro, Frank, Lupton, Michelle K., Martin, Nicholas G., Castelao, Enrique, Räikkönen, Katri, Eriksson, Johan G., Lahti, Jari, Hartman, Catharina A., Oldehinkel, Albertine J., Snieder, Harold, Liu, Hexuan, Preisig, Martin, Whipp, Alyce, Vuoksimaa, Eero, Lu, Yi, Jern, Patrick, Rujescu, Dan, Giegling, Ina, Palviainen, Teemu, Kaprio, Jaakko, Harden, Kathryn Paige, Munafò, Marcus R., Morneau-Vaillancourt, Geneviève, Plomin, Robert, Viding, Essi, Boutwell, Brian B., Aliev, Fazil, Dick, Danielle M., Popma, Arne, Faraone, Stephen V., Børglum, Anders D., Medland, Sarah E., Franke, Barbara, Boivin, Michel, Pingault, Jean-Baptiste, Glennon, Jeffrey C., Barnes, J. C., Fisher, Simon E., Moffitt, Terrie E., Caspi, Avshalom, Polderman, Tinca J. C., and Posthuma, Danielle

Published
2022
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14. Changing genetic architecture of body mass index from infancy to early adulthood: an individual based pooled analysis of 25 twin cohorts

Author

Silventoinen, Karri, Li, Weilong, Jelenkovic, Aline, Sund, Reijo, Yokoyama, Yoshie, Aaltonen, Sari, Piirtola, Maarit, Sugawara, Masumi, Tanaka, Mami, Matsumoto, Satoko, Baker, Laura A., Tuvblad, Catherine, Tynelius, Per, Rasmussen, Finn, Craig, Jeffrey M., Saffery, Richard, Willemsen, Gonneke, Bartels, Meike, van Beijsterveldt, Catharina E. M., Martin, Nicholas G., Medland, Sarah E., Montgomery, Grant W., Lichtenstein, Paul, Krueger, Robert F., McGue, Matt, Pahlen, Shandell, Christensen, Kaare, Skytthe, Axel, Kyvik, Kirsten O., Saudino, Kimberly J., Dubois, Lise, Boivin, Michel, Brendgen, Mara, Dionne, Ginette, Vitaro, Frank, Ullemar, Vilhelmina, Almqvist, Catarina, Magnusson, Patrik K. E., Corley, Robin P., Huibregtse, Brooke M., Knafo-Noam, Ariel, Mankuta, David, Abramson, Lior, Haworth, Claire M. A., Plomin, Robert, Bjerregaard-Andersen, Morten, Beck-Nielsen, Henning, Sodemann, Morten, Duncan, Glen E., Buchwald, Dedra, Burt, S. Alexandra, Klump, Kelly L., Llewellyn, Clare H., Fisher, Abigail, Boomsma, Dorret I., Sørensen, Thorkild I. A., and Kaprio, Jaakko

Published
2022
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15. Publisher Correction: Common schizophrenia alleles are enriched in mutation-intolerant genes and in regions under strong background selection

Author

Pardiñas, Antonio F, Holmans, Peter, Pocklington, Andrew J, Escott-Price, Valentina, Ripke, Stephan, Carrera, Noa, Legge, Sophie E, Bishop, Sophie, Cameron, Darren, Hamshere, Marian L, Han, Jun, Hubbard, Leon, Lynham, Amy, Mantripragada, Kiran, Rees, Elliott, MacCabe, James H, McCarroll, Steven A, Baune, Bernhard T, Breen, Gerome, Byrne, Enda M, Dannlowski, Udo, Eley, Thalia C, Hayward, Caroline, Martin, Nicholas G, McIntosh, Andrew M, Plomin, Robert, Porteous, David J, Wray, Naomi R, Caballero, Armando, Geschwind, Daniel H, Huckins, Laura M, Ruderfer, Douglas M, Santiago, Enrique, Sklar, Pamela, Stahl, Eli A, Won, Hyejung, Agerbo, Esben, Als, Thomas D, Andreassen, Ole A, Bækvad-Hansen, Marie, Mortensen, Preben Bo, Pedersen, Carsten Bøcker, Børglum, Anders D, Bybjerg-Grauholm, Jonas, Djurovic, Srdjan, Durmishi, Naser, Pedersen, Marianne Giørtz, Golimbet, Vera, Grove, Jakob, Hougaard, David M, Mattheisen, Manuel, Molden, Espen, Mors, Ole, Nordentoft, Merete, Pejovic-Milovancevic, Milica, Sigurdsson, Engilbert, Silagadze, Teimuraz, Hansen, Christine Søholm, Stefansson, Kari, Stefansson, Hreinn, Steinberg, Stacy, Tosato, Sarah, Werge, Thomas, Collier, David A, Rujescu, Dan, Kirov, George, Owen, Michael J, O’Donovan, Michael C, and Walters, James TR

Subjects
GERAD1 Consortium, CRESTAR Consortium, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Published
2019

16. Population‐based identity‐by‐descent mapping combined with exome sequencing to detect rare risk variants for schizophrenia

Author

Harold, Denise, Connolly, Siobhan, Riley, Brien P, Kendler, Kenneth S, McCarthy, Shane E, McCombie, William R, Richards, Alex, Owen, Michael J, O'Donovan, Michael C, Walters, James, Donnelly, Peter, Bates, Lesley, Barroso, Ines, Blackwell, Jenefer M, Bramon, Elvira, Brown, Matthew A, Casas, Juan P, Corvin, Aiden, Deloukas, Panos, Duncanson, Audrey, Jankowski, Janusz, Markus, Hugh S, Mathew, Christopher G, Palmer, Colin NA, Plomin, Robert, Rautanen, Anna, Sawcer, Stephen J, Trembath, Richard C, Viswanathan, Ananth C, Wood, Nicholas W, Spencer, Chris CA, Band, Gavin, Bellenguez, Céline, Freeman, Colin, Hellenthal, Garrett, Giannoulatou, Eleni, Hopkins, Lucinda, Pirinen, Matti, Pearson, Richard, Strange, Amy, Su, Zhan, Vukcevic, Damjan, Langford, Cordelia, Hunt, Sarah E, Edkins, Sarah, Gwilliam, Rhian, Blackburn, Hannah, Bumpstead, Suzannah J, Dronov, Serge, Gillman, Matthew, Gray, Emma, Hammond, Naomi, Jayakumar, Alagurevathi, McCann, Owen T, Liddle, Jennifer, Potter, Simon C, Ravindrarajah, Radhi, Ricketts, Michelle, Waller, Matthew, Weston, Paul, Widaa, Sara, Whittaker, Pamela, Ripke, Stephan, Neale, Benjamin M, Walters, James TR, Farh, Kai‐How, Holmans, Peter A, Lee, Phil, Bulik‐Sullivan, Brendan, Collier, David A, Huang, Hailiang, Pers, Tune H, Agartz, Ingrid, Agerbo, Esben, Albus, Margot, Alexander, Madeline, Amin, Farooq, Bacanu, Silviu A, Begemann, Martin, Belliveau, Richard A, Bene, Judit, Bergen, Sarah E, Bevilacqua, Elizabeth, Bigdeli, Tim B, Black, Donald W, Bruggeman, Richard, Buccola, Nancy G, Buckner, Randy L, Byerley, William, Cahn, Wiepke, Cai, Guiqing, Campion, Dominique, Cantor, Rita M, Carr, Vaughan J, Carrera, Noa, Catts, Stanley V, Chambert, Kimberley D, Chan, Raymond CK, and Chan, Ronald YL

Subjects
Biological Sciences, Genetics, Clinical Research, Schizophrenia, Brain Disorders, Human Genome, Prevention, Serious Mental Illness, Mental Health, Aetiology, 2.1 Biological and endogenous factors, Adult, Case-Control Studies, Chromosome Mapping, DNA Copy Number Variations, Databases, Genetic, Exome, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Haplotypes, Humans, Male, Middle Aged, Risk Factors, Sequence Analysis, DNA, Exome Sequencing, GWAS, IBD mapping, rare variants, Wellcome Trust Case Control Consortium 2, Schizophrenia Working Group of the Psychiatric Genomics Consortium, Clinical Sciences, Neurosciences, Clinical sciences
Abstract

Genome-wide association studies (GWASs) are highly effective at identifying common risk variants for schizophrenia. Rare risk variants are also important contributors to schizophrenia etiology but, with the exception of large copy number variants, are difficult to detect with GWAS. Exome and genome sequencing, which have accelerated the study of rare variants, are expensive so alternative methods are needed to aid detection of rare variants. Here we re-analyze an Irish schizophrenia GWAS dataset (n = 3,473) by performing identity-by-descent (IBD) mapping followed by exome sequencing of individuals identified as sharing risk haplotypes to search for rare risk variants in coding regions. We identified 45 rare haplotypes (>1 cM) that were significantly more common in cases than controls. By exome sequencing 105 haplotype carriers, we investigated these haplotypes for functional coding variants that could be tested for association in independent GWAS samples. We identified one rare missense variant in PCNT but did not find statistical support for an association with schizophrenia in a replication analysis. However, IBD mapping can prioritize both individual samples and genomic regions for follow-up analysis but genome rather than exome sequencing may be more effective at detecting risk variants on rare haplotypes.

Published
2019

18. Overview of CAPICE—Childhood and Adolescence Psychopathology: unravelling the complex etiology by a large Interdisciplinary Collaboration in Europe—an EU Marie Skłodowska-Curie International Training Network

Author

Rajula, Hema Sekhar Reddy, Manchia, Mirko, Agarwal, Kratika, Akingbuwa, Wonuola A., Allegrini, Andrea G., Diemer, Elizabeth, Doering, Sabrina, Haan, Elis, Jami, Eshim S., Karhunen, Ville, Leone, Marica, Schellhas, Laura, Thompson, Ashley, van den Berg, Stéphanie M., Bergen, Sarah E., Kuja-Halkola, Ralf, Hammerschlag, Anke R., Järvelin, Marjo Riitta, Leval, Amy, Lichtenstein, Paul, Lundstrom, Sebastian, Mauri, Matteo, Munafò, Marcus R., Myers, David, Plomin, Robert, Rimfeld, Kaili, Tiemeier, Henning, Ystrom, Eivind, Fanos, Vassilios, Bartels, Meike, and Middeldorp, Christel M.

Published
2022
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20. Nonshared environment: Real but random.

Author

Plomin, Robert

Subjects
*BEHAVIOR genetics, *PHILOSOPHY of science, *BIOLOGICAL systems, *SOMATIC mutation, *NATURE & nurture
Abstract

Background: In the excitement about genomics, it is easy to lose sight of one of the most important findings from behavioural genetics: At least half of the variance of psychopathology is caused by environmental effects that are not shared by children growing up in the same family, which includes error of measurement. However, a 30‐year search for the systematic causes of nonshared environment in a line‐up of the usual suspects, especially parenting, has not identified the culprits. Method: I briefly review this research, but primarily consider the conceptual framework of the search for 'missing' nonshared environmental effects. Results: The search has focused on exogenous events like parenting, but nonshared environment might not be caused by anything we would call an event. Instead, it might reflect endogenous processes such as noisy biological systems (such as somatic mutations and epigenetics) or, at a psychological level, idiosyncratic subjective perceptions of past and present experiences, which could be called nonshared environmental experience to distinguish it from exogenous events. Although real, nonshared environment might be random in the philosophy of science sense of being unpredictable, even though it can have stable effects that predict subsequent behaviour. Conclusion: I wade into the weeds of randomness and suggest that this so‐called 'gloomy prospect' might not be so gloomy. [ABSTRACT FROM AUTHOR]

Published
2024
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21. Nonshared Environmental Influences on Academic Achievement at Age 16: A Qualitative Hypothesis-Generating Monozygotic-Twin Differences Study

Author

Asbury, Kathryn, Moran, Nicola, and Plomin, Robert

Abstract

Twin studies find ~20% of the variance in achievement in public examinations taken at age 16 in the United Kingdom can be explained by experiences not shared within families. Nonshared environmental (NSE) influences, including measurement error, explain why monozygotic (MZ) twins differ from each other. Such influences work independently of genetic effects and may represent strong candidates for intervention. This study aimed to generate hypotheses about what these NSE factors might be. Perceptions of within-pair differences were gathered from n = 497 pairs of MZ twins and their parents, and telephone interviews were conducted with n = 56 families reporting different General Certificate of Secondary Education grades. "Environmental" explanations related to teacher quality, teacher-pupil relationships, and ability grouping. Families also explained discordance in terms of effort, interest, ability, and personality.

Published
2016

22. Preschool Verbal and Nonverbal Ability Mediate the Association between Socioeconomic Status and School Performance

Author

Stumm, Sophie, Rimfeld, Kaili, Dale, Philip S., and Plomin, Robert

Abstract

We compared the extent to which the long-term influence of family socioeconomic status (SES) on children's school performance from age 7 through 16 years was mediated by their preschool verbal and nonverbal ability. In 661 British children, who completed 17 researcher-administered ability tests at age 4.5 years, SES correlated more strongly with verbal than nonverbal ability (0.39 vs. 0.26). Verbal ability mediated about half of the association between SES and school performance at age 7, while nonverbal ability accounted for a third of the link. Only SES, but not verbal or nonverbal ability, was associated with changes in school performance from age 7 to 16. We found that SES-related differences in school performance are only partly transmitted through children's preschool verbal abilities.

Published
2020
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25. Common schizophrenia alleles are enriched in mutation-intolerant genes and in regions under strong background selection

Author

Pardiñas, Antonio F, Holmans, Peter, Pocklington, Andrew J, Escott-Price, Valentina, Ripke, Stephan, Carrera, Noa, Legge, Sophie E, Bishop, Sophie, Cameron, Darren, Hamshere, Marian L, Han, Jun, Hubbard, Leon, Lynham, Amy, Mantripragada, Kiran, Rees, Elliott, MacCabe, James H, McCarroll, Steven A, Baune, Bernhard T, Breen, Gerome, Byrne, Enda M, Dannlowski, Udo, Eley, Thalia C, Hayward, Caroline, Martin, Nicholas G, McIntosh, Andrew M, Plomin, Robert, Porteous, David J, Wray, Naomi R, Caballero, Armando, Geschwind, Daniel H, Huckins, Laura M, Ruderfer, Douglas M, Santiago, Enrique, Sklar, Pamela, Stahl, Eli A, Won, Hyejung, Agerbo, Esben, Als, Thomas D, Andreassen, Ole A, Bækvad-Hansen, Marie, Mortensen, Preben Bo, Pedersen, Carsten Bøcker, Børglum, Anders D, Bybjerg-Grauholm, Jonas, Djurovic, Srdjan, Durmishi, Naser, Pedersen, Marianne Giørtz, Golimbet, Vera, Grove, Jakob, Hougaard, David M, Mattheisen, Manuel, Molden, Espen, Mors, Ole, Nordentoft, Merete, Pejovic-Milovancevic, Milica, Sigurdsson, Engilbert, Silagadze, Teimuraz, Hansen, Christine Søholm, Stefansson, Kari, Stefansson, Hreinn, Steinberg, Stacy, Tosato, Sarah, Werge, Thomas, GERAD1 Consortium, CRESTAR Consortium, Collier, David A, Rujescu, Dan, Kirov, George, Owen, Michael J, O’Donovan, Michael C, and Walters, James TR

Subjects
Serious Mental Illness, Brain Disorders, Human Genome, Genetics, Mental Health, Biotechnology, Schizophrenia, 2.1 Biological and endogenous factors, Aetiology, Mental health, Good Health and Well Being, Alleles, Case-Control Studies, Gene Frequency, Genes, Lethal, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Inheritance Patterns, Polymorphism, Single Nucleotide, Selection, Genetic, GERAD1 Consortium, CRESTAR Consortium, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Schizophrenia is a debilitating psychiatric condition often associated with poor quality of life and decreased life expectancy. Lack of progress in improving treatment outcomes has been attributed to limited knowledge of the underlying biology, although large-scale genomic studies have begun to provide insights. We report a new genome-wide association study of schizophrenia (11,260 cases and 24,542 controls), and through meta-analysis with existing data we identify 50 novel associated loci and 145 loci in total. Through integrating genomic fine-mapping with brain expression and chromosome conformation data, we identify candidate causal genes within 33 loci. We also show for the first time that the common variant association signal is highly enriched among genes that are under strong selective pressures. These findings provide new insights into the biology and genetic architecture of schizophrenia, highlight the importance of mutation-intolerant genes and suggest a mechanism by which common risk variants persist in the population.

Published
2018

26. Anxiety symptom trajectories across development: risk factors and outcomes

Author

Palaiologou, Elisavet, primary, Skelton, Megan, additional, Assary, Elham, additional, Breen, Gerome, additional, Hotopf, Matthew, additional, Morneau-Vaillancourt, Geneviève, additional, Thompson, Ellen Jo, additional, Lockhart, Celestine Laetitia, additional, McGregor, Thomas, additional, Plomin, Robert, additional, Carr, Ewan, additional, and Eley, Thalia Catherine, additional

Published
2024
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28. Using DNA to Predict Educational Trajectories in Early Adulthood

Author

Ayorech, Ziada, Plomin, Robert, and von Stumm, Sophie

Abstract

At the end of compulsory schooling, young adults decide on educational and occupational trajectories that impact their subsequent employability, health and even life expectancy. To understand the antecedents to these decisions, we follow a new approach that considers genetic contributions, which have largely been ignored before. Using genomewide polygenic scores (EA3) from the most recent genomewide association study of years of education in 1.1 million individuals, we tested for genetic influence on early adult decisions in a United Kingdom--representative sample of 5,839 at 18 years of age. EA3 significantly predicted educational trajectories in early adulthood (Nagelkerke R[superscript 2] = 10%), ?[superscript 2](4) = 571.77, p < 0.001, indicating that young adults partly adapt their aspirations to their genetic propensities--a concept known as gene--environment correlation. Compared to attending university, a 1 standard deviation increase in EA3 was associated on average with a 51% reduction in the odds of pursuing full-time employment (OR = 0.47; 95% CI [0.43, 0.51]); an apprenticeship (OR = 0.49; 95% CI [0.45, 0.54]); or not going in education, employment, or training (OR = 0.50; 95% CI [0.41, 0.60]). EA3 associations were attenuated when controlling for previous academic achievement and family socioeconomic status. Overall this research illustrates how DNA-based predictions offer novel opportunities for studying the sociodevelopmental structures of life outcomes.

Published
2019
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35. Stability and Change in Genetic and Environmental Influences on Well-Being in Response to an Intervention.

Author

Haworth, Claire MA, Nelson, S Katherine, Layous, Kristin, Carter, Kathryn, Jacobs Bao, Katherine, Lyubomirsky, Sonja, and Plomin, Robert

Subjects
Humans, Models, Statistical, Case-Control Studies, Mental Health, Mental Disorders, Psychiatric Status Rating Scales, Health Status, Twins, Dizygotic, Twins, Monozygotic, Phenotype, Adolescent, Early Intervention (Education), Female, Male, Gene-Environment Interaction, Surveys and Questionnaires, General Science & Technology
Abstract

Genetic and environmental influences on complex traits can change in response to developmental and environmental contexts. Here we explore the impact of a positive activity intervention on the genetic and environmental influences on well-being and mental health in a sample of 750 adolescent twins. Twins completed a 10-week online well-being intervention, consisting of kindness and gratitude tasks and matched control activities. The results showed significant improvements both in well-being and in internalizing symptoms in response to the intervention activities. We used multivariate twin analyses of repeated measures, tracking stability and change in genetic and environmental influences, to assess the impact of this environmental intervention on these variance components. The heritability of well-being remained high both before and after the intervention, and the same genetic effects were important at each stage, even as well-being increased. The overall magnitude of environmental influences was also stable across the intervention; however, different non-shared environmental influences emerged during the intervention. Our study highlights the value of exploring the innovations in non-shared environmental influences that could provide clues to the mechanisms behind improvements in well-being. The findings also emphasize that even traits strongly influenced by genetics, like well-being, are subject to change in response to environmental interventions.

Published
2016

37. Genome-wide association study meta-analysis of dizygotic twinning illuminates genetic regulation of female fecundity

Author

Mbarek, Hamdi, primary, Gordon, Scott D, additional, Duffy, David L, additional, Hubers, Nikki, additional, Mortlock, Sally, additional, Beck, Jeffrey J, additional, Hottenga, Jouke-Jan, additional, Pool, René, additional, Dolan, Conor V, additional, Actkins, Ky’Era V, additional, Gerring, Zachary F, additional, Van Dongen, Jenny, additional, Ehli, Erik A, additional, Iacono, William G, additional, Mcgue, Matt, additional, Chasman, Daniel I, additional, Gallagher, C Scott, additional, Schilit, Samantha L P, additional, Morton, Cynthia C, additional, Paré, Guillaume, additional, Willemsen, Gonneke, additional, Whiteman, David C, additional, Olsen, Catherine M, additional, Derom, Catherine, additional, Vlietinck, Robert, additional, Gudbjartsson, Daniel, additional, Cannon-Albright, Lisa, additional, Krapohl, Eva, additional, Plomin, Robert, additional, Magnusson, Patrik K E, additional, Pedersen, Nancy L, additional, Hysi, Pirro, additional, Mangino, Massimo, additional, Spector, Timothy D, additional, Palviainen, Teemu, additional, Milaneschi, Yuri, additional, Penninnx, Brenda W, additional, Campos, Adrian I, additional, Ong, Ken K, additional, Perry, John R B, additional, Lambalk, Cornelis B, additional, Kaprio, Jaakko, additional, Ólafsson, Ísleifur, additional, Duroure, Karine, additional, Revenu, Céline, additional, Rentería, Miguel E, additional, Yengo, Loic, additional, Davis, Lea, additional, Derks, Eske M, additional, Medland, Sarah E, additional, Stefansson, Hreinn, additional, Stefansson, Kari, additional, Del Bene, Filippo, additional, Reversade, Bruno, additional, Montgomery, Grant W, additional, Boomsma, Dorret I, additional, and Martin, Nicholas G, additional

Published
2023
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38. Genome-wide analyses of vocabulary size in infancy and toddlerhood: associations with ADHD, literacy and cognition-related traits

Author

Verhoef, Ellen, primary, Allegrini, Andrea G., additional, Jansen, Philip R., additional, Lange, Katherine, additional, Wang, Carol A., additional, Morgan, Angela T., additional, Ahluwalia, Tarunveer S., additional, Symeonides, Christos, additional, Eising, Else, additional, Franken, Marie-Christine, additional, Hypponen, Elina, additional, Mansell, Toby, additional, Olislagers, Mitchell, additional, Omerovic, Emina, additional, Rimfeld, Kaili, additional, Schlag, Fenja, additional, Selzam, Saskia, additional, Shapland, Chin Yang, additional, Tiemeier, Henning, additional, Whitehouse, Andrew J.O., additional, Saffery, Richard, additional, Bønnelykke, Klaus, additional, Reilly, Sheena, additional, Pennell, Craig E., additional, Wake, Melissa, additional, Cecil, Charlotte A.M., additional, Plomin, Robert, additional, Fisher, Simon E., additional, St Pourcain, Beate, additional, Andreassen, Ole A., additional, Bartels, Meike, additional, Boomsma, Dorret, additional, Dale, Philip S., additional, Ehli, Erik, additional, Fernandez-Orth, Dietmar, additional, Guxens, Mònica, additional, Hakulinen, Christian, additional, Harris, Kathleen Mullan, additional, Haworth, Simon, additional, de Hoyos, Lucía, additional, Jaddoe, Vincent, additional, Keltikangas-Järvinen, Liisa, additional, Lehtimäki, Terho, additional, Middeldorp, Christel, additional, Min, Josine L., additional, Mishra, Pashupati P., additional, Njølstad, Pål Rasmus, additional, Sunyer, Jordi, additional, Tate, Ashley E., additional, Timpson, Nicholas, additional, van der Laan, Camiel, additional, Vrijheid, Martine, additional, Vuoksimaa, Eero, additional, Whipp, Alyce, additional, and Ystrom, Eivind, additional

Published
2023
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40. Genetic association study of childhood aggression across raters, instruments, and age

Author

Ip, Hill F., van der Laan, Camiel M., Krapohl, Eva M. L., Brikell, Isabell, Sánchez-Mora, Cristina, Nolte, Ilja M., St Pourcain, Beate, Bolhuis, Koen, Palviainen, Teemu, Zafarmand, Hadi, Colodro-Conde, Lucía, Gordon, Scott, Zayats, Tetyana, Aliev, Fazil, Jiang, Chang, Wang, Carol A., Saunders, Gretchen, Karhunen, Ville, Hammerschlag, Anke R., Adkins, Daniel E., Border, Richard, Peterson, Roseann E., Prinz, Joseph A., Thiering, Elisabeth, Seppälä, Ilkka, Vilor-Tejedor, Natàlia, Ahluwalia, Tarunveer S., Day, Felix R., Hottenga, Jouke-Jan, Allegrini, Andrea G., Rimfeld, Kaili, Chen, Qi, Lu, Yi, Martin, Joanna, Soler Artigas, María, Rovira, Paula, Bosch, Rosa, Español, Gemma, Ramos Quiroga, Josep Antoni, Neumann, Alexander, Ensink, Judith, Grasby, Katrina, Morosoli, José J., Tong, Xiaoran, Marrington, Shelby, Middeldorp, Christel, Scott, James G., Vinkhuyzen, Anna, Shabalin, Andrey A., Corley, Robin, Evans, Luke M., Sugden, Karen, Alemany, Silvia, Sass, Lærke, Vinding, Rebecca, Ruth, Kate, Tyrrell, Jess, Davies, Gareth E., Ehli, Erik A., Hagenbeek, Fiona A., De Zeeuw, Eveline, Van Beijsterveldt, Toos C.E.M., Larsson, Henrik, Snieder, Harold, Verhulst, Frank C., Amin, Najaf, Whipp, Alyce M., Korhonen, Tellervo, Vuoksimaa, Eero, Rose, Richard J., Uitterlinden, André G., Heath, Andrew C., Madden, Pamela, Haavik, Jan, Harris, Jennifer R., Helgeland, Øyvind, Johansson, Stefan, Knudsen, Gun Peggy S., Njolstad, Pal Rasmus, Lu, Qing, Rodriguez, Alina, Henders, Anjali K., Mamun, Abdullah, Najman, Jackob M., Brown, Sandy, Hopfer, Christian, Krauter, Kenneth, Reynolds, Chandra, Smolen, Andrew, Stallings, Michael, Wadsworth, Sally, Wall, Tamara L., Silberg, Judy L., Miller, Allison, Keltikangas-Järvinen, Liisa, Hakulinen, Christian, Pulkki-Råback, Laura, Havdahl, Alexandra, Magnus, Per, Raitakari, Olli T., Perry, John R. B., Llop, Sabrina, Lopez-Espinosa, Maria-Jose, Bønnelykke, Klaus, Bisgaard, Hans, Sunyer, Jordi, Lehtimäki, Terho, Arseneault, Louise, Standl, Marie, Heinrich, Joachim, Boden, Joseph, Pearson, John, Horwood, L. John, Kennedy, Martin, Poulton, Richie, Eaves, Lindon J., Maes, Hermine H., Hewitt, John, Copeland, William E., Costello, Elizabeth J., Williams, Gail M., Wray, Naomi, Järvelin, Marjo-Riitta, McGue, Matt, Iacono, William, Caspi, Avshalom, Moffitt, Terrie E., Whitehouse, Andrew, Pennell, Craig E., Klump, Kelly L., Burt, S. Alexandra, Dick, Danielle M., Reichborn-Kjennerud, Ted, Martin, Nicholas G., Medland, Sarah E., Vrijkotte, Tanja, Kaprio, Jaakko, Tiemeier, Henning, Davey Smith, George, Hartman, Catharina A., Oldehinkel, Albertine J., Casas, Miquel, Ribasés, Marta, Lichtenstein, Paul, Lundström, Sebastian, Plomin, Robert, Bartels, Meike, Nivard, Michel G., and Boomsma, Dorret I.

Published
2021
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43. Monozygotic Twin Differences in School Performance Are Stable and Systematic

Author

von Stumm, Sophie and Plomin, Robert

Abstract

School performance is one of the most stable and heritable psychological characteristics. Notwithstanding, monozygotic twins (MZ), who have identical genotypes, differ in school performance. These MZ differences result from non-shared environments that do not contribute to the similarity within twin pairs. Because to date few non-shared environmental factors have been reliably associated with MZ differences in school performance, they are thought to be idiosyncratic and due to chance, suggesting that the effect of non-shared environments on MZ differences are age- and trait-specific. In a sample of 2768 MZ twin pairs, we found first that MZ differences in school performance were moderately stable from age 12 through 16, with differences at the ages 12 and 14 accounting for 20% of the variance in MZ differences at age 16. Second, MZ differences in school performance correlated positively with MZ differences across 16 learning-related variables, including measures of intelligence, personality and school attitudes, with the twin who scored higher on one also scoring higher on the other measures. Finally, MZ differences in the 16 learning-related variables accounted for 22% of the variance in MZ differences in school performance at age 16. These findings suggest that, unlike for other psychological domains, non-shared environmental factors affect school performance in systematic ways that have long-term and generalist influence. Our findings should motivate the search for non-shared environmental factors responsible for the stable and systematic effects on children's differences in school performance.

Published
2018
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44. Face Identity Recognition and the Social Difficulties Component of the Autism-Like Phenotype: Evidence for Phenotypic and Genetic Links

Author

Lewis, Gary J., Shakeshaft, Nicolas G., and Plomin, Robert

Abstract

Autism spectrum disorder (ASD) and autism-like traits are associated with deficits in face memory ability, although it is not yet clear whether this deficit reflects a specific aspect of the ASD/autism-like phenotype. We addressed this issue using a neurotypical sample of adolescent twins (N[subscript complete pairs] = 782) drawn from the Twins Early Development Study who were assessed on face and object memory performance alongside two core aspects of autism-like traits: (i) difficulties with social behavior/interactions, and (ii) attention to detail. We observed a negative association between face memory ability and difficulties with social behavior/interactions. This association reflected an overlapping genetic etiology: heritable influences acting on face memory ability are associated with the social difficulties aspects of autism-like traits.

Published
2018
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50. The Genetic Architecture of Oral Language, Reading Fluency, and Reading Comprehension: A Twin Study from 7 to 16 Years

Author

Tosto, Maria G., Hayiou-Thomas, Marianna E., Harlaar, Nicole, Prom-Wormley, Elizabeth, Dale, Philip S., and Plomin, Robert

Abstract

This study examines the genetic and environmental etiology underlying the development of oral language and reading skills, and the relationship between them, over a long period of developmental time spanning middle childhood and adolescence. It focuses particularly on the differential relationship between language and two different aspects of reading: reading fluency and reading comprehension. Structural equation models were applied to language and reading data at 7, 12, and 16 years from the large-scale TEDS twin study. A series of multivariate twin models show a clear patterning of oral language with reading comprehension, as distinct from reading fluency: significant but moderate genetic overlap between oral language and reading fluency (genetic correlation r[subscript g] = 0.46-0.58 at 7, 12, and 16) contrasts with very substantial genetic overlap between oral language and reading comprehension (r[subscript g] = 0.81-0.87, at 12 and 16). This pattern is even clearer in a latent factors model, fit to the data aggregated across ages, in which a single factor representing oral language and reading comprehension is correlated with--but distinct from--a second factor representing reading fluency. A distinction between oral language and reading fluency is also apparent in different developmental trajectories: While the heritability of oral language increases over the period from 7 to 12 to 16 years (from h[superscript 2] = 0.27 to 0.47 to 0.55), the heritability of reading fluency is high and largely stable over the same period of time (h[superscript 2] = 0.73 to 0.71 to 0.64).

Published
2017
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