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51. Identifying Cortical Structure Markers of Resilience to Adversity in Young People using Surface-Based Morphometry

Author

Cornwell, Harriet, primary, Toschi, Nicola, additional, Hamilton-Giachritsis, Catherine, additional, Staginnus, Marlene, additional, Smaragdi, Areti, additional, Gonzalez-Madruga, Karen, additional, Mackes, Nuria, additional, Rogers, Jack, additional, Martinelli, Anne, additional, Kohls, Gregor, additional, Raschle, Nora Maria, additional, Konrad, Kerstin, additional, Stadler, Christina, additional, Freitag, Christine M, additional, De Brito, Stephane A, additional, and Fairchild, Graeme, additional

Published
2024
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52. Phase-IIa randomized, double-blind, sham-controlled, parallel group trial on anodal transcranial direct current stimulation (tDCS) over the left and right tempo-parietal junction in autism spectrum disorder—StimAT: study protocol for a clinical trial

Author

Luckhardt, Christina, Schütz, Magdalena, Mühlherr, Andreas, Mössinger, Hannah, Boxhoorn, Sara, Dempfle, Astrid, Salvador, Ricardo, Ruffini, Giulio, Pereira, Helena C., Castelo-Branco, Miguel, Latinus, Marianne, Bonnet-Brilhault, Frédérique, Siemann, Julia, Siniatchkin, Michael, Ecker, Christine, and Freitag, Christine M.

Published
2021
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53. Author Correction: Altered structural brain asymmetry in autism spectrum disorder in a study of 54 datasets

Author

Postema, Merel C., van Rooij, Daan, Anagnostou, Evdokia, Arango, Celso, Auzias, Guillaume, Behrmann, Marlene, Filho, Geraldo Busatto, Calderoni, Sara, Calvo, Rosa, Daly, Eileen, Deruelle, Christine, Di Martino, Adriana, Dinstein, Ilan, Duran, Fabio Luis S., Durston, Sarah, Ecker, Christine, Ehrlich, Stefan, Fair, Damien, Fedor, Jennifer, Feng, Xin, Fitzgerald, Jackie, Floris, Dorothea L., Freitag, Christine M., Gallagher, Louise, Glahn, David C., Gori, Ilaria, Haar, Shlomi, Hoekstra, Liesbeth, Jahanshad, Neda, Jalbrzikowski, Maria, Janssen, Joost, King, Joseph A., Kong, Xiang Zhen, Lazaro, Luisa, Lerch, Jason P., Luna, Beatriz, Martinho, Mauricio M., McGrath, Jane, Medland, Sarah E., Muratori, Filippo, Murphy, Clodagh M., Murphy, Declan G. M., O’Hearn, Kirsten, Oranje, Bob, Parellada, Mara, Puig, Olga, Retico, Alessandra, Rosa, Pedro, Rubia, Katya, Shook, Devon, Taylor, Margot J., Tosetti, Michela, Wallace, Gregory L., Zhou, Fengfeng, Thompson, Paul M., Fisher, Simon E., Buitelaar, Jan K., and Francks, Clyde

Published
2021
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54. Correction: SLC25A24 gene methylation and gray matter volume in females with and without conduct disorder: an exploratory epigenetic neuroimaging study

Author

Farrow, Elizabeth, Chiocchetti, Andreas G., Rogers, Jack C., Pauli, Ruth, Raschle, Nora M., Gonzalez-Madruga, Karen, Smaragdi, Areti, Martinelli, Anne, Kohls, Gregor, Stadler, Christina, Konrad, Kerstin, Fairchild, Graeme, Freitag, Christine M., Chechlacz, Magdalena, and De Brito, Stephane A.

Published
2021
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56. White Matter Microstructure in Youths With Conduct Disorder: Effects of Sex and Variation in Callous Traits

Author

Rogers, Jack C., Gonzalez-Madruga, Karen, Kohls, Gregor, Baker, Rosalind H., Clanton, Roberta L., Pauli, Ruth, Birch, Philippa, Chowdhury, Alimul I., Kirchner, Marietta, Andersson, Jesper L.R., Smaragdi, Areti, Puzzo, Ignazio, Baumann, Sarah, Raschle, Nora M., Fehlbaum, Lynn V., Menks, Willeke M., Steppan, Martin, Stadler, Christina, Konrad, Kerstin, Freitag, Christine M., Fairchild, Graeme, and De Brito, Stephane A.

Published
2019
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66. Does helping mothers in multigenerational ADHD also help children in the long run? 2-year follow-up from baseline of the AIMAC randomized controlled multicentre trial

Author

Geissler, Julia M., Vloet, Timo D., Strom, Nora, Jaite, Charlotte, Graf, Erika, Kappel, Viola, Warnke, Andreas, Jacob, Christian, Hennighausen, Klaus, Haack-Dees, Barbara, Schneider-Momm, Katja, Matthies, Swantje, Rösler, Michael, Retz, Wolfgang, Hänig, Susann, von Gontard, Alexander, Sobanski, Esther, Alm, Barbara, Hohmann, Sarah, Poustka, Luise, Colla, Michael, Gentschow, Laura, Freitag, Christine M., Häge, Alexander, Holtmann, Martin, Becker, Katja, Philipsen, Alexandra, and Jans, Thomas

Published
2020
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69. Baseline autonomic nervous system activity in female children and adolescents with conduct disorder: Psychophysiological findings from the FemNAT-CD study

Author

Oldenhof, Helena, Prätzlich, Martin, Ackermann, Katharina, Baker, Rosalind, Batchelor, Molly, Baumann, Sarah, Bernhard, Anka, Clanton, Roberta, Dikeos, Dimitris, Dochnal, Roberta, Fehlbaum, Lynn Valérie, Fernández-Rivas, Aranzazu, de Geus, Eco, Gonzalez, Karen, de Artaza-Lavesa, Maider González, Guijarro, Silvina, Gundlach, Malou, Herpertz-Dahlmann, Beate, Hervas, Amaia, Jansen, Lucres, Kersten, Linda, Kohls, Gregor, Konsta, Angeliki, Lazaratou, Helen, Kerexeta-Lizeaga, Iñaki, Martinelli, Anne, van Nimwegen, Tisse, Puzzo, Ignazio, Raschle, Nora Maria, Rogers, Jack, Siklósi, Réka, Smaragdi, Areti, Steppan, Martin, De Brito, Stephane, Fairchild, Graeme, Kieser, Meinhard, Konrad, Kerstin, Freitag, Christine, Stadler, Christina, and Popma, Arne

Published
2019
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70. Resting autonomic nervous system activity is unrelated to antisocial behaviour dimensions in adolescents: Cross-sectional findings from a European multi-centre study

Author

Prätzlich, Martin, Oldenhof, Helena, Steppan, Martin, Ackermann, Katharina, Baker, Rosalind, Batchelor, Molly, Baumann, Sarah, Bernhard, Anka, Clanton, Roberta, Dikeos, Dimitris, Dochnal, Roberta, Fehlbaum, Lynn Valérie, Fernández-Rivas, Aranzazu, González de Artaza-Lavesa, Maider, Gonzalez-Madruga, Karen, Guijarro, Silvina, Gundlach, Malou, Herpertz-Dahlmann, Beate, Hervas, Amaia, Jansen, Lucres, Kerexeta-Lizeaga, Iñaki, Kersten, Linda, Kirchner, Marietta, Kohls, Gregor, Konsta, Angeliki, Lazaratou, Helen, Martinelli, Anne, Menks, Willeke Martine, Puzzo, Ignazio, Raschle, Nora Maria, Rogers, Jack, Siklósi, Réka, Smaragdi, Areti, Vriends, Noortje, Konrad, Kerstin, De Brito, Stephane, Fairchild, Graeme, Kieser, Meinhard, Freitag, Christine M., Popma, Arne, and Stadler, Christina

Published
2019
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74. Cortical structure and subcortical volumes in conduct disorder: a coordinated analysis of 15 international cohorts from the ENIGMA-Antisocial Behavior Working Group

Author

Gao, Yidian, Staginnus, Marlene, Gao, Yidian, Staginnus, Marlene, Townend, Sophie, Arango, Celso, Bajaj, Sahil, Banaschewski, Tobias, Barker, Edward D., Benegal, Vivek, Berluti, Kathryn, Bernhard, Anka, Blair, Robert J.R., Boateng, Charlotte P.S., Bokde, Arun L.W., Brandeis, Daniel, Buitelaar, Jan K., Burt, S. Alexandra, Cardinale, Elise M., Castro-Fornieles, Josefina, Chen, Hui, Chen, Xianliang, Chester, Sally C., Colins, Olivier F., Cornwell, Harriet, Craig, Michael, Cubillo, Ana I., Desrivieres, Sylvane, Díaz, Dana E., Dietrich, Andrea, Dong, Daifeng, Dykstra, Anouk H., Franke, Barbara, Freitag, Christine M., Glennon, Jeffrey C., Gonzalez-Madruga, Karen, Hagan, Cindy C., Hoekstra, Pieter J., Holla, Bharath, Hyde, Luke W., Ibrahim, Karim, Jabeen, Nimrah, Jackson, Rebecca L., Jiang, Yali, Kohls, Gregor, Konrad, Kerstin, Kypta-Vivanco, Alexandra, Lamers, Kim, Ma, Ren, Marsh, Abigail A., Martinelli, Anne, Martinot, Jean-Luc, Michalska, Kalina J., Ming, Qingsen, Minosse, Silvia, Mitchell, Colter, Monk, Christopher S., Murphy, Declan, Mycue, Leah E., Naaijen, Jilly, Oosterling, Maaike, Passamonti, Luca, Pauli, Ruth, Penzol Alonso, Maria Jose, Phillips, Harriet, Ploe, Montana L., Raschle, Nora M., Roberts, Ruth, Rogers, Jack C., Rosa-Justicia, Mireia, Sagar-Ouriaghli, Ilyas, Schulze, Ulrike M.E., Schumann, Gunter, Sethi, Arjun, Smaragdi, Areti, Sonuga-Barke, Edmund J.S., Stadler, Christina, Stevens, Michael C., Sukhodolsky, Denis G., Sully, Kate, Sun, Xiaoqiang, Toschi, Nicola, Townsend, Christopher D., van der Wee, Nic J.A., Vermeiren, Robert, Viding, Essi, Wang, Xiaoping, Westerman, Heidi B., Wu, Qiong, Yao, Shuqiao, Zhang, Jibiao, Zhou, Jiansong, Zhou, Jiawei, Jahanshad, Neda, Thomopoulos, Sophia I., Ching, Christopher R.K., Kang, Melody J.Y., Thompson, Paul M., Klapwijk, Eduard T., Pine, Daniel S., Baskin-Sommers, Arielle, Cecil, Charlotte A.M., Aghajani, Moji, Walton, Esther, Fairchild, Graeme, and De Brito, Stephane A.

Abstract

Conduct disorder is associated with the highest burden of any mental disorder in childhood, yet its neurobiology remains unclear. Inconsistent findings limit our understanding of the role of brain structure alterations in conduct disorder. This study aims to identify the most robust and replicable brain structural correlates of conduct disorder.

Published
2024
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77. Convergence of Genes and Cellular Pathways Dysregulated in Autism Spectrum Disorders

Author

Pinto, Dalila, Delaby, Elsa, Merico, Daniele, Barbosa, Mafalda, Merikangas, Alison, Klei, Lambertus, Thiruvahindrapuram, Bhooma, Xu, Xiao, Ziman, Robert, Wang, Zhuozhi, Vorstman, Jacob AS, Thompson, Ann, Regan, Regina, Pilorge, Marion, Pellecchia, Giovanna, Pagnamenta, Alistair T, Oliveira, Bárbara, Marshall, Christian R, Magalhaes, Tiago R, Lowe, Jennifer K, Howe, Jennifer L, Griswold, Anthony J, Gilbert, John, Duketis, Eftichia, Dombroski, Beth A, De Jonge, Maretha V, Cuccaro, Michael, Crawford, Emily L, Correia, Catarina T, Conroy, Judith, Conceição, Inês C, Chiocchetti, Andreas G, Casey, Jillian P, Cai, Guiqing, Cabrol, Christelle, Bolshakova, Nadia, Bacchelli, Elena, Anney, Richard, Gallinger, Steven, Cotterchio, Michelle, Casey, Graham, Zwaigenbaum, Lonnie, Wittemeyer, Kerstin, Wing, Kirsty, Wallace, Simon, van Engeland, Herman, Tryfon, Ana, Thomson, Susanne, Soorya, Latha, Rogé, Bernadette, Roberts, Wendy, Poustka, Fritz, Mouga, Susana, Minshew, Nancy, McInnes, L Alison, McGrew, Susan G, Lord, Catherine, Leboyer, Marion, Le Couteur, Ann S, Kolevzon, Alexander, González, Patricia Jiménez, Jacob, Suma, Holt, Richard, Guter, Stephen, Green, Jonathan, Green, Andrew, Gillberg, Christopher, Fernandez, Bridget A, Duque, Frederico, Delorme, Richard, Dawson, Geraldine, Chaste, Pauline, Café, Cátia, Brennan, Sean, Bourgeron, Thomas, Bolton, Patrick F, Bölte, Sven, Bernier, Raphael, Baird, Gillian, Bailey, Anthony J, Anagnostou, Evdokia, Almeida, Joana, Wijsman, Ellen M, Vieland, Veronica J, Vicente, Astrid M, Schellenberg, Gerard D, Pericak-Vance, Margaret, Paterson, Andrew D, Parr, Jeremy R, Oliveira, Guiomar, Nurnberger, John I, Monaco, Anthony P, Maestrini, Elena, Klauck, Sabine M, Hakonarson, Hakon, Haines, Jonathan L, Geschwind, Daniel H, Freitag, Christine M, Folstein, Susan E, and Ennis, Sean

Subjects
Genetics, Brain Disorders, Pediatric, Mental Health, Intellectual and Developmental Disabilities (IDD), Neurosciences, Autism, 2.1 Biological and endogenous factors, Aetiology, Child, Child Development Disorders, Pervasive, DNA Copy Number Variations, Female, Gene Regulatory Networks, Humans, Male, Metabolic Networks and Pathways, Multigene Family, Pedigree, Sequence Deletion, Biological Sciences, Medical and Health Sciences, Genetics & Heredity
Abstract

Rare copy-number variation (CNV) is an important source of risk for autism spectrum disorders (ASDs). We analyzed 2,446 ASD-affected families and confirmed an excess of genic deletions and duplications in affected versus control groups (1.41-fold, p = 1.0 × 10(-5)) and an increase in affected subjects carrying exonic pathogenic CNVs overlapping known loci associated with dominant or X-linked ASD and intellectual disability (odds ratio = 12.62, p = 2.7 × 10(-15), ∼3% of ASD subjects). Pathogenic CNVs, often showing variable expressivity, included rare de novo and inherited events at 36 loci, implicating ASD-associated genes (CHD2, HDAC4, and GDI1) previously linked to other neurodevelopmental disorders, as well as other genes such as SETD5, MIR137, and HDAC9. Consistent with hypothesized gender-specific modulators, females with ASD were more likely to have highly penetrant CNVs (p = 0.017) and were also overrepresented among subjects with fragile X syndrome protein targets (p = 0.02). Genes affected by de novo CNVs and/or loss-of-function single-nucleotide variants converged on networks related to neuronal signaling and development, synapse function, and chromatin regulation.

Published
2014

78. The Autism Simplex Collection: an international, expertly phenotyped autism sample for genetic and phenotypic analyses

Author

Buxbaum, Joseph D, Bolshakova, Nadia, Brownfeld, Jessica M, Anney, Richard JL, Bender, Patrick, Bernier, Raphael, Cook, Edwin H, Coon, Hilary, Cuccaro, Michael, Freitag, Christine M, Hallmayer, Joachim, Geschwind, Daniel, Klauck, Sabine M, Nurnberger, John I, Oliveira, Guiomar, Pinto, Dalila, Poustka, Fritz, Scherer, Stephen W, Shih, Andy, Sutcliffe, James S, Szatmari, Peter, Vicente, Astrid M, Vieland, Veronica, and Gallagher, Louise

Subjects
Intellectual and Developmental Disabilities (IDD), Clinical Research, Brain Disorders, Pediatric, Autism, Mental Health, Genetics, Behavioral and Social Science, Human Genome, Mental health, Good Health and Well Being, Clinical Sciences, Neurosciences
Abstract

BackgroundThere is an urgent need for expanding and enhancing autism spectrum disorder (ASD) samples, in order to better understand causes of ASD.MethodsIn a unique public-private partnership, 13 sites with extensive experience in both the assessment and diagnosis of ASD embarked on an ambitious, 2-year program to collect samples for genetic and phenotypic research and begin analyses on these samples. The program was called The Autism Simplex Collection (TASC). TASC sample collection began in 2008 and was completed in 2010, and included nine sites from North America and four sites from Western Europe, as well as a centralized Data Coordinating Center.ResultsOver 1,700 trios are part of this collection, with DNA from transformed cells now available through the National Institute of Mental Health (NIMH). Autism Diagnostic Interview-Revised (ADI-R) and Autism Diagnostic Observation Schedule-Generic (ADOS-G) measures are available for all probands, as are standardized IQ measures, Vineland Adaptive Behavioral Scales (VABS), the Social Responsiveness Scale (SRS), Peabody Picture Vocabulary Test (PPVT), and physical measures (height, weight, and head circumference). At almost every site, additional phenotypic measures were collected, including the Broad Autism Phenotype Questionnaire (BAPQ) and Repetitive Behavior Scale-Revised (RBS-R), as well as the non-word repetition scale, Communication Checklist (Children's or Adult), and Aberrant Behavior Checklist (ABC). Moreover, for nearly 1,000 trios, the Autism Genome Project Consortium (AGP) has carried out Illumina 1 M SNP genotyping and called copy number variation (CNV) in the samples, with data being made available through the National Institutes of Health (NIH). Whole exome sequencing (WES) has been carried out in over 500 probands, together with ancestry matched controls, and this data is also available through the NIH. Additional WES is being carried out by the Autism Sequencing Consortium (ASC), where the focus is on sequencing complete trios. ASC sequencing for the first 1,000 samples (all from whole-blood DNA) is complete and data will be released in 2014. Data is being made available through NIH databases (database of Genotypes and Phenotypes (dbGaP) and National Database for Autism Research (NDAR)) with DNA released in Dist 11.0. Primary funding for the collection, genotyping, sequencing and distribution of TASC samples was provided by Autism Speaks and the NIH, including the National Institute of Mental Health (NIMH) and the National Human Genetics Research Institute (NHGRI).ConclusionsTASC represents an important sample set that leverages expert sites. Similar approaches, leveraging expert sites and ongoing studies, represent an important path towards further enhancing available ASD samples.

Published
2014

79. START NOW: a cognitive behavioral skills training for adolescent girls with conduct or oppositional defiant disorder – a randomized clinical trial.

Author

Stadler, Christina, Freitag, Christine M., Popma, Arne, Nauta‐Jansen, Lucres, Konrad, Kerstin, Unternaehrer, Eva, Ackermann, Katharina, Bernhard, Anka, Martinelli, Anne, Oldenhof, Helena, Gundlach, Malou, Kohls, Gregor, Prätzlich, Martin, Kieser, Meinhard, Limprecht, Ronald, Raschle, Nora M., Vriends, Noortje, Trestman, Robert L., Kirchner, Marietta, and Kersten, Linda

Subjects
*RESEARCH, *CONFIDENCE intervals, *RESEARCH methodology, *PSYCHOSOCIAL functioning, *BEHAVIOR disorders, *PSYCHOLOGY of women, *OPPOSITIONAL defiant disorder in children, *AGGRESSION (Psychology), *COGNITIVE therapy, *MOTOR ability, *SOCIAL disabilities, *LONGITUDINAL method, *ADOLESCENCE
Abstract

Background: Conduct disorder (CD) and oppositional defiant disorder (ODD) both convey a high risk for maladjustment later in life and are understudied in girls. Here, we aimed at confirming the efficacy of START NOW, a cognitive‐behavioral, dialectical behavior therapy‐oriented skills training program aiming to enhance emotion regulation skills, interpersonal and psychosocial adjustment, adapted for female adolescents with CD or ODD. Methods: A total of 127 girls were included in this prospective, cluster randomized, multi‐center, parallel group, quasi‐randomized, controlled phase III trial, which tested the efficacy of START NOW (n = 72) compared with standard care (treatment as usual, TAU, n = 55). All female adolescents had a clinical diagnosis of CD or ODD, were 15.6 (±1.5) years on average (range: 12–20 years), and were institutionalized in youth welfare institutions. The two primary endpoints were the change in number of CD/ODD symptoms between (1) baseline (T1) and post‐treatment (T3), and (2) between T1 and 12‐week follow‐up (T4). Results: Both treatment groups showed reduced CD/ODD symptoms at T3 compared with T1 (95% CI: START NOW = −4.87, −2.49; TAU = −4.94, −2.30). There was no significant mean difference in CD/ODD symptom reduction from T1 to T3 between START NOW and TAU (−0.056; 95% CI = −1.860, 1.749; Hedge's g = −0.011). However, the START NOW group showed greater mean symptom reduction from T1 to T4 (−2.326; 95% CI = −4.274, −0.378; Hedge's g = −0.563). Additionally, secondary endpoint results revealed a reduction in staff reported aggression and parent‐reported irritability at post assessment. Conclusions: Although START NOW did not result in greater symptom reduction from baseline to post‐treatment compared with TAU, the START NOW group showed greater symptom reduction from baseline to follow‐up with a medium effect size, which indicates a clinically meaningful delayed treatment effect. [ABSTRACT FROM AUTHOR]

Published
2024
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80. START NOW: a cognitive behavioral skills training for adolescent girls with conduct or oppositional defiant disorder – a randomized clinical trial

Author

Stadler, Christina, primary, Freitag, Christine M., additional, Popma, Arne, additional, Nauta‐Jansen, Lucres, additional, Konrad, Kerstin, additional, Unternaehrer, Eva, additional, Ackermann, Katharina, additional, Bernhard, Anka, additional, Martinelli, Anne, additional, Oldenhof, Helena, additional, Gundlach, Malou, additional, Kohls, Gregor, additional, Prätzlich, Martin, additional, Kieser, Meinhard, additional, Limprecht, Ronald, additional, Raschle, Nora M., additional, Vriends, Noortje, additional, Trestman, Robert L., additional, Kirchner, Marietta, additional, and Kersten, Linda, additional

Published
2023
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85. Neural Correlates of Explicit versus Implicit Facial Emotion Processing in ASD

Author

Luckhardt, Christina, Kröger, Anne, Cholemkery, Hannah, Bender, Stephan, and Freitag, Christine M.

Abstract

The underlying neural mechanisms of implicit and explicit facial emotion recognition (FER) were studied in children and adolescents with autism spectrum disorder (ASD) compared to matched typically developing controls (TDC). EEG was obtained from N = 21 ASD and N = 16 TDC. Task performance, visual (P100, N170) and cognitive (late positive potential) event-related-potentials, as well as coherence were compared across groups. TDC showed a task-dependent increase and a stronger lateralization of P100 amplitude during the explicit task and task-dependent modulation of intra-hemispheric coherence in the beta band. In contrast, the ASD group showed no task dependent modulation. Results indicate disruptions in early visual processing and top-down attentional processes as contributing factors to FER deficits in ASD.

Published
2017
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86. High Loading of Polygenic Risk for ADHD in Children With Comorbid Aggression

Author

Hamshere, Marian L, Langley, Kate, Martin, Joanna, Agha, Sharifah Shameem, Stergiakouli, Evangelia, Anney, Richard JL, Buitelaar, Jan, Faraone, Stephen V, Lesch, Klaus-Peter, Neale, Benjamin M, Franke, Barbara, Sonuga-Barke, Edmund, Asherson, Philip, Merwood, Andrew, Kuntsi, Jonna, Medland, Sarah E, Ripke, Stephan, Steinhausen, Hans-Christoph, Freitag, Christine, Reif, Andreas, Renner, Tobias J, Romanos, Marcel, Romanos, Jasmin, Warnke, Andreas, Meyer, Jobst, Palmason, Haukur, Vasquez, Alejandro Arias, Lambregts-Rommelse, Nanda, Roeyers, Herbert, Biederman, Joseph, Doyle, Alysa E, Hakonarson, Hakon, Rothenberger, Aribert, Banaschewski, Tobias, Oades, Robert D, McGough, James J, Kent, Lindsey, Williams, Nigel, Owen, Michael J, Holmans, Peter, O’Donovan, Michael C, and Thapar, Anita

Subjects
Prevention, Behavioral and Social Science, Human Genome, Genetics, Mental Health, Attention Deficit Hyperactivity Disorder (ADHD), Clinical Research, Brain Disorders, Pediatric, Aetiology, 2.1 Biological and endogenous factors, Mental health, Aggression, Anxiety Disorders, Attention Deficit Disorder with Hyperactivity, Child, Child, Preschool, Comorbidity, Conduct Disorder, Depressive Disorder, Female, Genetic Predisposition to Disease, Genetic Variation, Humans, Male, Multifactorial Inheritance, United Kingdom, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry
Abstract

OBJECTIVE Although attention deficit hyperactivity disorder (ADHD) is highly heritable, genome-wide association studies (GWAS) have not yet identified any common genetic variants that contribute to risk. There is evidence that aggression or conduct disorder in children with ADHD indexes higher genetic loading and clinical severity. The authors examine whether common genetic variants considered en masse as polygenic scores for ADHD are especially enriched in children with comorbid conduct disorder. METHOD Polygenic scores derived from an ADHD GWAS meta-analysis were calculated in an independent ADHD sample (452 case subjects, 5,081 comparison subjects). Multivariate logistic regression analyses were employed to compare polygenic scores in the ADHD and comparison groups and test for higher scores in ADHD case subjects with comorbid conduct disorder relative to comparison subjects and relative to those without comorbid conduct disorder. Association with symptom scores was tested using linear regression. RESULTS Polygenic risk for ADHD, derived from the meta-analysis, was higher in the independent ADHD group than in the comparison group. Polygenic score was significantly higher in ADHD case subjects with conduct disorder relative to ADHD case subjects without conduct disorder. ADHD polygenic score showed significant association with comorbid conduct disorder symptoms. This relationship was explained by the aggression items. CONCLUSIONS Common genetic variation is relevant to ADHD, especially in individuals with comorbid aggression. The findings suggest that the previously published ADHD GWAS meta-analysis contains weak but true associations with common variants, support for which falls below genome-wide significance levels. The findings also highlight the fact that aggression in ADHD indexes genetic as well as clinical severity.

Published
2013

88. Relational Aggression in Adolescents with Conduct Disorder: Sex Differences and Behavioral Correlates

Author

Ackermann, Katharina, Kirchner, Marietta, Bernhard, Anka, Martinelli, Anne, Anomitri, Chrysanthi, Baker, Rosalind, Baumann, Sarah, Dochnal, Roberta, Fernandez-Rivas, Aranzazu, Gonzalez-Madruga, Karen, Herpertz-Dahlmann, Beate, Hervas, Amaia, Jansen, Lucres, Kapornai, Kristina, Kersten, Linda, Kohls, Gregor, Limprecht, Ronald, Lazaratou, Helen, McLaughlin, Ana, Oldenhof, Helena, Rogers, Jack C., Siklósi, Réka, Smaragdi, Areti, Vivanco-Gonzalez, Esther, Stadler, Christina, Fairchild, Graeme, Popma, Arne, De Brito, Stephane A., Konrad, Kerstin, and Freitag, Christine M.

Published
2019
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90. Recessive gene disruptions in autism spectrum disorder

Author

Doan, Ryan N., Lim, Elaine T., De Rubeis, Silvia, Betancur, Catalina, Cutler, David J., Chiocchetti, Andreas G., Overman, Lynne M., Soucy, Aubrie, Goetze, Susanne, Autism Sequencing Consortium, Freitag, Christine M., Daly, Mark J., Walsh, Christopher A., Buxbaum, Joseph D., and Yu, Timothy W.

Published
2019
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92. A novel approach of homozygous haplotype sharing identifies candidate genes in autism spectrum disorder

Author

Casey, Jillian P, Magalhaes, Tiago, Conroy, Judith M, Regan, Regina, Shah, Naisha, Anney, Richard, Shields, Denis C, Abrahams, Brett S, Almeida, Joana, Bacchelli, Elena, Bailey, Anthony J, Baird, Gillian, Battaglia, Agatino, Berney, Tom, Bolshakova, Nadia, Bolton, Patrick F, Bourgeron, Thomas, Brennan, Sean, Cali, Phil, Correia, Catarina, Corsello, Christina, Coutanche, Marc, Dawson, Geraldine, de Jonge, Maretha, Delorme, Richard, Duketis, Eftichia, Duque, Frederico, Estes, Annette, Farrar, Penny, Fernandez, Bridget A, Folstein, Susan E, Foley, Suzanne, Fombonne, Eric, Freitag, Christine M, Gilbert, John, Gillberg, Christopher, Glessner, Joseph T, Green, Jonathan, Guter, Stephen J, Hakonarson, Hakon, Holt, Richard, Hughes, Gillian, Hus, Vanessa, Igliozzi, Roberta, Kim, Cecilia, Klauck, Sabine M, Kolevzon, Alexander, Lamb, Janine A, Leboyer, Marion, Le Couteur, Ann, Leventhal, Bennett L, Lord, Catherine, Lund, Sabata C, Maestrini, Elena, Mantoulan, Carine, Marshall, Christian R, McConachie, Helen, McDougle, Christopher J, McGrath, Jane, McMahon, William M, Merikangas, Alison, Miller, Judith, Minopoli, Fiorella, Mirza, Ghazala K, Munson, Jeff, Nelson, Stanley F, Nygren, Gudrun, Oliveira, Guiomar, Pagnamenta, Alistair T, Papanikolaou, Katerina, Parr, Jeremy R, Parrini, Barbara, Pickles, Andrew, Pinto, Dalila, Piven, Joseph, Posey, David J, Poustka, Annemarie, Poustka, Fritz, Ragoussis, Jiannis, Roge, Bernadette, Rutter, Michael L, Sequeira, Ana F, Soorya, Latha, Sousa, Inês, Sykes, Nuala, Stoppioni, Vera, Tancredi, Raffaella, Tauber, Maïté, Thompson, Ann P, Thomson, Susanne, Tsiantis, John, Van Engeland, Herman, Vincent, John B, Volkmar, Fred, Vorstman, Jacob AS, Wallace, Simon, Wang, Kai, Wassink, Thomas H, White, Kathy, and Wing, Kirsty

Subjects
Autism, Genetics, Mental Health, Intellectual and Developmental Disabilities (IDD), Brain Disorders, Biotechnology, Pediatric, Human Genome, Aetiology, 2.1 Biological and endogenous factors, Mental health, Adult, Child, Child Development Disorders, Pervasive, Cluster Analysis, Cohort Studies, DNA Copy Number Variations, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Haplotypes, Homozygote, Humans, Linkage Disequilibrium, Male, Middle Aged, Nuclear Family, Polymorphism, Single Nucleotide, Complementary and Alternative Medicine, Paediatrics and Reproductive Medicine, Genetics & Heredity
Abstract

Autism spectrum disorder (ASD) is a highly heritable disorder of complex and heterogeneous aetiology. It is primarily characterized by altered cognitive ability including impaired language and communication skills and fundamental deficits in social reciprocity. Despite some notable successes in neuropsychiatric genetics, overall, the high heritability of ASD (~90%) remains poorly explained by common genetic risk variants. However, recent studies suggest that rare genomic variation, in particular copy number variation, may account for a significant proportion of the genetic basis of ASD. We present a large scale analysis to identify candidate genes which may contain low-frequency recessive variation contributing to ASD while taking into account the potential contribution of population differences to the genetic heterogeneity of ASD. Our strategy, homozygous haplotype (HH) mapping, aims to detect homozygous segments of identical haplotype structure that are shared at a higher frequency amongst ASD patients compared to parental controls. The analysis was performed on 1,402 Autism Genome Project trios genotyped for 1 million single nucleotide polymorphisms (SNPs). We identified 25 known and 1,218 novel ASD candidate genes in the discovery analysis including CADM2, ABHD14A, CHRFAM7A, GRIK2, GRM3, EPHA3, FGF10, KCND2, PDZK1, IMMP2L and FOXP2. Furthermore, 10 of the previously reported ASD genes and 300 of the novel candidates identified in the discovery analysis were replicated in an independent sample of 1,182 trios. Our results demonstrate that regions of HH are significantly enriched for previously reported ASD candidate genes and the observed association is independent of gene size (odds ratio 2.10). Our findings highlight the applicability of HH mapping in complex disorders such as ASD and offer an alternative approach to the analysis of genome-wide association data.

Published
2012

93. Genome-Wide Analysis of Copy Number Variants in Attention Deficit Hyperactivity Disorder: The Role of Rare Variants and Duplications at 15q13.3

Author

Williams, Nigel M, Franke, Barbara, Mick, Eric, Anney, Richard JL, Freitag, Christine M, Gill, Michael, Thapar, Anita, O'Donovan, Michael C, Owen, Michael J, Holmans, Peter, Kent, Lindsey, Middleton, Frank, Zhang-James, Yanli, Liu, Lu, Meyer, Jobst, Nguyen, Thuy Trang, Romanos, Jasmin, Romanos, Marcel, Seitz, Christiane, Renner, Tobias J, Walitza, Susanne, Warnke, Andreas, Palmason, Haukur, Buitelaar, Jan, Rommelse, Nanda, Vasquez, Alejandro Arias, Hawi, Ziarih, Langley, Kate, Sergeant, Joseph, Steinhausen, Hans-Christoph, Roeyers, Herbert, Biederman, Joseph, Zaharieva, Irina, Hakonarson, Hakon, Elia, Josephine, Lionel, Anath C, Crosbie, Jennifer, Marshall, Christian R, Schachar, Russell, Scherer, Stephen W, Todorov, Alexandre, Smalley, Susan L, Loo, Sandra, Nelson, Stanley, Shtir, Corina, Asherson, Philip, Reif, Andreas, Lesch, Klaus-Peter, and Faraone, Stephen V

Subjects
Human Genome, Clinical Research, Mental Health, Genetics, Pediatric, Attention Deficit Hyperactivity Disorder (ADHD), Brain Disorders, Serious Mental Illness, 2.1 Biological and endogenous factors, Aetiology, Adolescent, Attention Deficit Disorder with Hyperactivity, Canada, Causality, Child, Child, Preschool, Female, Gene Dosage, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, In Situ Hybridization, Fluorescence, Inheritance Patterns, Polymorphism, Single Nucleotide, Receptors, Nicotinic, Segmental Duplications, Genomic, United Kingdom, United States, alpha7 Nicotinic Acetylcholine Receptor, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry
Abstract

ObjectiveAttention deficit hyperactivity disorder (ADHD) is a common, highly heritable psychiatric disorder. Because of its multifactorial etiology, however, identifying the genes involved has been difficult. The authors followed up on recent findings suggesting that rare copy number variants (CNVs) may be important for ADHD etiology.MethodThe authors performed a genome-wide analysis of large, rare CNVs (100 kb in size, which segregated into 912 independent loci. Overall, the rate of rare CNVs >100 kb was 1.15 times higher in ADHD case subjects relative to comparison subjects, with duplications spanning known genes showing a 1.2-fold enrichment. In accordance with a previous study, rare CNVs >500 kb showed the greatest enrichment (1.28-fold). CNVs identified in ADHD case subjects were significantly enriched for loci implicated in autism and in schizophrenia. Duplications spanning the CHRNA7 gene at chromosome 15q13.3 were associated with ADHD in single-locus analysis. This finding was consistently replicated in an additional 2,242 ADHD case subjects and 8,552 comparison subjects from four independent cohorts from the United Kingdom, the United States, and Canada. Presence of the duplication at 15q13.3 appeared to be associated with comorbid conduct disorder.ConclusionsThese findings support the enrichment of large, rare CNVs in ADHD and implicate duplications at 15q13.3 as a novel risk factor for ADHD. With a frequency of 0.6% in the populations investigated and a relatively large effect size (odds ratio=2.22, 95% confidence interval=1.5–3.6), this locus could be an important contributor to ADHD etiology.

Published
2012

95. The role of rare compound heterozygous events in autism spectrum disorder

Author

Lin, Bochao Danae, Colas, Fabrice, Nijman, Isaac J., Medic, Jelena, Brands, William, Parr, Jeremy R., van Eijk, Kristel R., Klauck, Sabine M., Chiocchetti, Andreas G., Freitag, Christine M., Maestrini, Elena, Bacchelli, Elena, Coon, Hilary, Vicente, Astrid, Oliveira, Guiomar, Pagnamenta, Alistair T., Gallagher, Louise, Ennis, Sean, Anney, Richard, Bourgeron, Thomas, Luykx, Jurjen J., and Vorstman, Jacob

Published
2020
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96. A genome-wide scan for common alleles affecting risk for autism

Author

Anney, Richard, Klei, Lambertus, Pinto, Dalila, Regan, Regina, Conroy, Judith, Magalhaes, Tiago R, Correia, Catarina, Abrahams, Brett S, Sykes, Nuala, Pagnamenta, Alistair T, Almeida, Joana, Bacchelli, Elena, Bailey, Anthony J, Baird, Gillian, Battaglia, Agatino, Berney, Tom, Bolshakova, Nadia, Bölte, Sven, Bolton, Patrick F, Bourgeron, Thomas, Brennan, Sean, Brian, Jessica, Carson, Andrew R, Casallo, Guillermo, Casey, Jillian, Chu, Su H, Cochrane, Lynne, Corsello, Christina, Crawford, Emily L, Crossett, Andrew, Dawson, Geraldine, de Jonge, Maretha, Delorme, Richard, Drmic, Irene, Duketis, Eftichia, Duque, Frederico, Estes, Annette, Farrar, Penny, Fernandez, Bridget A, Folstein, Susan E, Fombonne, Eric, Freitag, Christine M, Gilbert, John, Gillberg, Christopher, Glessner, Joseph T, Goldberg, Jeremy, Green, Jonathan, Guter, Stephen J, Hakonarson, Hakon, Heron, Elizabeth A, Hill, Matthew, Holt, Richard, Howe, Jennifer L, Hughes, Gillian, Hus, Vanessa, Igliozzi, Roberta, Kim, Cecilia, Klauck, Sabine M, Kolevzon, Alexander, Korvatska, Olena, Kustanovich, Vlad, Lajonchere, Clara M, Lamb, Janine A, Laskawiec, Magdalena, Leboyer, Marion, Le Couteur, Ann, Leventhal, Bennett L, Lionel, Anath C, Liu, Xiao-Qing, Lord, Catherine, Lotspeich, Linda, Lund, Sabata C, Maestrini, Elena, Mahoney, William, Mantoulan, Carine, Marshall, Christian R, McConachie, Helen, McDougle, Christopher J, McGrath, Jane, McMahon, William M, Melhem, Nadine M, Merikangas, Alison, Migita, Ohsuke, Minshew, Nancy J, Mirza, Ghazala K, Munson, Jeff, Nelson, Stanley F, Noakes, Carolyn, Noor, Abdul, Nygren, Gudrun, Oliveira, Guiomar, Papanikolaou, Katerina, Parr, Jeremy R, Parrini, Barbara, Paton, Tara, Pickles, Andrew, Piven, Joseph, Posey, David J, Poustka, Annemarie, and Poustka, Fritz

Subjects
Clinical Research, Human Genome, Mental Health, Genetics, Brain Disorders, Pediatric, Biotechnology, Intellectual and Developmental Disabilities (IDD), Autism, Prevention, Aetiology, 2.1 Biological and endogenous factors, Alleles, Autistic Disorder, DNA Copy Number Variations, Databases, Genetic, Genetic Predisposition to Disease, Genetic Variation, Genome, Human, Genome-Wide Association Study, Genotype, Humans, Polymorphism, Single Nucleotide, Risk Factors, White People, Biological Sciences, Medical and Health Sciences, Genetics & Heredity
Abstract

Although autism spectrum disorders (ASDs) have a substantial genetic basis, most of the known genetic risk has been traced to rare variants, principally copy number variants (CNVs). To identify common risk variation, the Autism Genome Project (AGP) Consortium genotyped 1558 rigorously defined ASD families for 1 million single-nucleotide polymorphisms (SNPs) and analyzed these SNP genotypes for association with ASD. In one of four primary association analyses, the association signal for marker rs4141463, located within MACROD2, crossed the genome-wide association significance threshold of P < 5 × 10(-8). When a smaller replication sample was analyzed, the risk allele at rs4141463 was again over-transmitted; yet, consistent with the winner's curse, its effect size in the replication sample was much smaller; and, for the combined samples, the association signal barely fell below the P < 5 × 10(-8) threshold. Exploratory analyses of phenotypic subtypes yielded no significant associations after correction for multiple testing. They did, however, yield strong signals within several genes, KIAA0564, PLD5, POU6F2, ST8SIA2 and TAF1C.

Published
2010

97. Linking heart rate variability to psychological health and brain structure in adolescents with and without conduct disorder

Author

Cubillo, Ana, primary, Tkalcec, Antonia, additional, Oldenhof, Helena, additional, Unternaehrer, Eva, additional, Raschle, Nora, additional, Kohls, Gregor, additional, Nauta-Jansen, Lucres, additional, Hervas, Amaia, additional, Fernandez-Rivas, Aranzazu, additional, Konrad, Kerstin, additional, Popma, Arne, additional, Freitag, Christine, additional, de Brito, Stephane, additional, Fairchild, Graeme, additional, and Stadler, Christina, additional

Published
2023
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98. The clinical and molecular spectrum of the KDM6B-related neurodevelopmental disorder

Author

Rots, Dmitrijs, primary, Jakub, Taryn E., additional, Keung, Crystal, additional, Jackson, Adam, additional, Banka, Siddharth, additional, Pfundt, Rolph, additional, de Vries, Bert B.A., additional, van Jaarsveld, Richard H., additional, Hopman, Saskia M.J., additional, van Binsbergen, Ellen, additional, Valenzuela, Irene, additional, Hempel, Maja, additional, Bierhals, Tatjana, additional, Kortüm, Fanny, additional, Lecoquierre, Francois, additional, Goldenberg, Alice, additional, Hertz, Jens Michael, additional, Andersen, Charlotte Brasch, additional, Kibæk, Maria, additional, Prijoles, Eloise J., additional, Stevenson, Roger E., additional, Everman, David B., additional, Patterson, Wesley G., additional, Meng, Linyan, additional, Gijavanekar, Charul, additional, De Dios, Karl, additional, Lakhani, Shenela, additional, Levy, Tess, additional, Wagner, Matias, additional, Wieczorek, Dagmar, additional, Benke, Paul J., additional, Lopez Garcia, María Soledad, additional, Perrier, Renee, additional, Sousa, Sergio B., additional, Almeida, Pedro M., additional, Simões, Maria José, additional, Isidor, Bertrand, additional, Deb, Wallid, additional, Schmanski, Andrew A., additional, Abdul-Rahman, Omar, additional, Philippe, Christophe, additional, Bruel, Ange-Line, additional, Faivre, Laurence, additional, Vitobello, Antonio, additional, Thauvin, Christel, additional, Smits, Jeroen J., additional, Garavelli, Livia, additional, Caraffi, Stefano G., additional, Peluso, Francesca, additional, Davis-Keppen, Laura, additional, Platt, Dylan, additional, Royer, Erin, additional, Leeuwen, Lisette, additional, Sinnema, Margje, additional, Stegmann, Alexander P.A., additional, Stumpel, Constance T.R.M., additional, Tiller, George E., additional, Bosch, Daniëlle G.M., additional, Potgieter, Stephanus T., additional, Joss, Shelagh, additional, Splitt, Miranda, additional, Holden, Simon, additional, Prapa, Matina, additional, Foulds, Nicola, additional, Douzgou, Sofia, additional, Puura, Kaija, additional, Waltes, Regina, additional, Chiocchetti, Andreas G., additional, Freitag, Christine M., additional, Satterstrom, F. Kyle, additional, De Rubeis, Silvia, additional, Buxbaum, Joseph, additional, Gelb, Bruce D., additional, Branko, Aleksic, additional, Kushima, Itaru, additional, Howe, Jennifer, additional, Scherer, Stephen W., additional, Arado, Alessia, additional, Baldo, Chiara, additional, Patat, Olivier, additional, Bénédicte, Demeer, additional, Lopergolo, Diego, additional, Santorelli, Filippo M., additional, Haack, Tobias B., additional, Dufke, Andreas, additional, Bertrand, Miriam, additional, Falb, Ruth J., additional, Rieß, Angelika, additional, Krieg, Peter, additional, Spranger, Stephanie, additional, Bedeschi, Maria Francesca, additional, Iascone, Maria, additional, Josephi-Taylor, Sarah, additional, Roscioli, Tony, additional, Buckley, Michael F., additional, Liebelt, Jan, additional, Dagli, Aditi I., additional, Aten, Emmelien, additional, Hurst, Anna C.E., additional, Hicks, Alesha, additional, Suri, Mohnish, additional, Aliu, Ermal, additional, Naik, Sunil, additional, Sidlow, Richard, additional, Coursimault, Juliette, additional, Nicolas, Gaël, additional, Küpper, Hanna, additional, Petit, Florence, additional, Ibrahim, Veyan, additional, Top, Deniz, additional, Di Cara, Francesca, additional, Louie, Raymond J., additional, Stolerman, Elliot, additional, Brunner, Han G., additional, Vissers, Lisenka E.L.M., additional, Kramer, Jamie M., additional, and Kleefstra, Tjitske, additional

Published
2023
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99. Autismus-Spektrum-Störungen

Author

Freitag, Christine, Jarczok, Tomasz, Gerlach, Manfred, editor, Mehler-Wex, Claudia, editor, Walitza, Susanne, editor, Warnke, Andreas, editor, and Wewetzer, Christoph, editor

Published
2016
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