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1. Consortium neuroscience of attention deficit/hyperactivity disorder and autism spectrum disorder

Author: Mara Parellada, Kerstin Konrad, Mark A. Bellgrove, Stefan Ehrlich, Thomas Frodl, Ruth O'Gorman Tuura, Evdokia Anagnostou, J. Antoni Ramos-Quiroga, David Coghill, Clyde Francks, Georgii Karkashadze, Damien A. Fair, Francisco X. Castellanos, Oscar Vilarroya, Eugenio H. Grevet, Yash Patel, Eileen Daly, Clodagh M. Murphy, Klaus-Peter Lesch, Kirsten O'Hearn, Claiton H.D. Bau, Jeffery N. Epstein, Daan van Rooij, Liesbeth Reneman, Eileen Oberwelland-Weiss, Timothy J. Silk, Yanli Zhang-James, Christine M. Freitag, Jane McGrath, Tomáš Paus, Jan Haavik, Louise Gallagher, Ting Li, Merel Postema, Celso Arango, Barbara Franke, Sara Calderoni, Jaap Oosterlaan, Andreas Reif, Paulo Mattos, Iva Ilioska, Leanne Tamm, Paul M. Thompson, Joost Janssen, Pieter J. Hoekstra, Neda Jahanshad, Jacqueline Fitzgerald, Odile A. van den Heuvel, Pedro G.P. Rosa, Tobias Banaschewski, Joseph A. King, Katya Rubia, Christine Deruelle, Marieke Klein, Stephen V. Faraone, Philip Shaw, Premika S.W. Boedhoe, Kerstin Jessica Plessen, Luisa Lázaro, Alessandra Retico, Jan K. Buitelaar, Paul Pauli, Guillaume Auzias, Joel T. Nigg, Christine Ecker, Annette Conzelmann, Jonna Kuntsi, Sarah Durston, Beatriz Luna, Silvia Brem, Marlene Behrmann, Jason P. Lerch, Susanne Walitza, Martine Hoogman, Filippo Muratori, Ilan Dinstein, Rosa Calvo, Mario Rodrigues Louzã, Geraldo F. Busatto, Daniel Brandeis, Institut de Neurosciences de la Timone (INT), and Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS)
Subjects: Neurology, Autism Spectrum Disorder, [SDV]Life Sciences [q-bio], CHILDREN, Review Article, 0302 clinical medicine, Transtorno do espectro autista, pathology [Brain], 130 000 Cognitive Neurology & Memory, GENETIC INFLUENCES, Neurociències, Multicenter Studies as Topic, Review Articles, Mapeamento encefálico, ComputingMilieux_MISCELLANEOUS, LIFE-SPAN, neuroimaging, Radiological and Ultrasound Technology, Consórcios de saúde, 05 social sciences, ENIGMA, Brain, 220 Statistical Imaging Neuroscience, Transtorno do déficit de atenção com hiperatividade, Autism spectrum disorders, Cerebral cortex, Trastorns de l'espectre autista, 3. Good health, IMAGING FINDINGS, Escorça cerebral, cortex, Autism spectrum disorder, Cortex, Trastorns per dèficit d'atenció amb hiperactivitat en els adults, Anatomy, Psychology, diagnostic imaging [Autism Spectrum Disorder], Clinical psychology, medicine.medical_specialty, DEFICIT HYPERACTIVITY DISORDER, BRAIN ABNORMALITIES, ADHD, ASD, subcortical volumes, Brain Structure and Function, Neuroimaging, pathology [Autism Spectrum Disorder], behavioral disciplines and activities, 050105 experimental psychology, 03 medical and health sciences, mental disorders, medicine, Attention deficit hyperactivity disorder, Humans, 0501 psychology and cognitive sciences, Radiology, Nuclear Medicine and imaging, ddc:610, diagnostic imaging [Brain], METAANALYSIS, Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], Neurosciences, pathology [Attention Deficit Disorder with Hyperactivity], medicine.disease, Mental health, Subcortical volumes, Attention Deficit Disorder with Hyperactivity, Attention deficit disorder with hyperactivity in adults, Autism, diagnostic imaging [Attention Deficit Disorder with Hyperactivity], Neurology (clinical), Working group, 170 000 Motivational & Cognitive Control, CORTICAL THICKNESS, 030217 neurology & neurosurgery
Abstract: Human brain mapping 43(1), 37-55 (2022). doi:10.1002/hbm.25029 special issue: "Special Issue: The ENIGMA Consortium: the first 10 years / Issue Edited by: P.M. Thompson, N. Jahanshad, L. Schmaal, J.A. Turner, A. Winkler, S.I. Thomopoulos, G.F. Egan, P. Kochunov", Published by Wiley-Liss, New York, NY
Published: 2022
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2. The role of glucocorticoid receptor gene in the association between attention deficit-hyperactivity disorder and smaller brain structures

Author: Claiton H.D. Bau, Maria Eduarda Tavares, Cibele Edom Bandeira, Eduardo S. Vitola, Eugenio H. Grevet, Renata B. Cupertino, Clara S Gusmão, Luis Augusto Rohde, Felipe Almeida Picon, Bruna Santos da Silva, Diego L. Rovaris, and Djenifer B. Kappel
Subjects: Regulation of gene expression, Linkage disequilibrium, medicine.medical_specialty, Neurology, business.industry, Nucleus accumbens, medicine.disease, Amygdala, Psychiatry and Mental health, Glucocorticoid receptor, medicine.anatomical_structure, Neuroimaging, mental disorders, Medicine, Attention deficit hyperactivity disorder, Neurology (clinical), business, Neuroscience, Biological Psychiatry
Abstract: ADHD is associated with smaller subcortical brain volumes and cortical surface area, with greater effects observed in children than adults. It is also associated with dysregulation of the HPA axis. Considering the effects of the glucocorticoid receptor (NR3C1) in neurophysiology, we hypothesize that the blurred relationships between brain structures and ADHD in adults could be partly explained by NR3C1 gene variation. Structural T1-weighted images were acquired on a 3 T scanner (N = 166). Large-scale genotyping was performed, and it was followed by quality control and pruning procedures, which resulted in 48 independent NR3C1 gene variants analyzed. After a stringent Bonferroni correction, two SNPs (rs2398631 and rs72801070) moderated the association between ADHD and accumbens and amygdala volumes in adults. The significant SNPs that interacted with ADHD appear to have a role in gene expression regulation, and they are in linkage disequilibrium with NR3C1 variants that present well-characterized physiological functions. The literature-reported associations of ADHD with accumbens and amygdala were only observed for specific NR3C1 genotypes. Our findings reinforce the influence of the NR3C1 gene on subcortical volumes and ADHD. They suggest a genetic modulation of the effects of a pivotal HPA axis component in the neuroanatomical features of ADHD.
Published: 2021
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3. Virtual Ontogeny of Cortical Growth Preceding Mental Illness

Author: Yash Patel, Jean Shin, Christoph Abé, Ingrid Agartz, Clara Alloza, Dag Alnæs, Sonia Ambrogi, Linda A. Antonucci, Celso Arango, Volker Arolt, Guillaume Auzias, Rosa Ayesa-Arriola, Nerisa Banaj, Tobias Banaschewski, Cibele Bandeira, Zeynep Başgöze, Renata Basso Cupertino, Claiton H.D. Bau, Jochen Bauer, Sarah Baumeister, Fabio Bernardoni, Alessandro Bertolino, Caterina del Mar Bonnin, Daniel Brandeis, Silvia Brem, Jason Bruggemann, Robin Bülow, Juan R. Bustillo, Sara Calderoni, Rosa Calvo, Erick J. Canales-Rodríguez, Dara M. Cannon, Susanna Carmona, Vaughan J. Carr, Stanley V. Catts, Sneha Chenji, Qian Hui Chew, David Coghill, Colm G. Connolly, Annette Conzelmann, Alexander R. Craven, Benedicto Crespo-Facorro, Kathryn Cullen, Andreas Dahl, Udo Dannlowski, Christopher G. Davey, Christine Deruelle, Covadonga M. Díaz-Caneja, Katharina Dohm, Stefan Ehrlich, Jeffery Epstein, Tracy Erwin-Grabner, Lisa T. Eyler, Jennifer Fedor, Jacqueline Fitzgerald, William Foran, Judith M. Ford, Lydia Fortea, Paola Fuentes-Claramonte, Janice Fullerton, Lisa Furlong, Louise Gallagher, Bingchen Gao, Si Gao, Jose M. Goikolea, Ian Gotlib, Roberto Goya-Maldonado, Hans J. Grabe, Melissa Green, Eugenio H. Grevet, Nynke A. Groenewold, Dominik Grotegerd, Oliver Gruber, Jan Haavik, Tim Hahn, Ben J. Harrison, Walter Heindel, Frans Henskens, Dirk J. Heslenfeld, Eva Hilland, Pieter J. Hoekstra, Sarah Hohmann, Nathalie Holz, Fleur M. Howells, Jonathan C. Ipser, Neda Jahanshad, Babette Jakobi, Andreas Jansen, Joost Janssen, Rune Jonassen, Anna Kaiser, Vasiliy Kaleda, James Karantonis, Joseph A. King, Tilo Kircher, Peter Kochunov, Sheri-Michelle Koopowitz, Mikael Landén, Nils Inge Landrø, Stephen Lawrie, Irina Lebedeva, Beatriz Luna, Astri J. Lundervold, Frank P. MacMaster, Luigi A. Maglanoc, Daniel H. Mathalon, Colm McDonald, Andrew McIntosh, Susanne Meinert, Patricia T. Michie, Philip Mitchell, Ana Moreno-Alcázar, Bryan Mowry, Filippo Muratori, Leila Nabulsi, Igor Nenadić, Ruth O'Gorman Tuura, Jaap Oosterlaan, Bronwyn Overs, Christos Pantelis, Mara Parellada, Jose C. Pariente, Paul Pauli, Giulio Pergola, Francesco Maria Piarulli, Felipe Picon, Fabrizio Piras, Edith Pomarol-Clotet, Clara Pretus, Yann Quidé, Joaquim Radua, J. Antoni Ramos-Quiroga, Paul E. Rasser, Andreas Reif, Alessandra Retico, Gloria Roberts, Susan Rossell, Diego Luiz Rovaris, Katya Rubia, Matthew D. Sacchet, Josep Salavert, Raymond Salvador, Salvador Sarró, Akira Sawa, Ulrich Schall, Rodney Scott, Pierluigi Selvaggi, Tim Silk, Kang Sim, Antonin Skoch, Gianfranco Spalletta, Filip Spaniel, Dan J. Stein, Olaf Steinsträter, Aleks Stolicyn, Yoichiro Takayanagi, Leanne Tamm, Maria Tavares, Alexander Teumer, Katharina Thiel, Sophia I. Thomopoulos, David Tomecek, Alexander S. Tomyshev, Diana Tordesillas-Gutiérrez, Michela Tosetti, Anne Uhlmann, Tamsyn Van Rheenen, Javier Vazquez-Bourgón, Meike W. Vernooij, Eduard Vieta, Oscar Vilarroya, Cynthia Weickert, Thomas Weickert, Lars T. Westlye, Heather Whalley, David Willinger, Alexandra Winter, Katharina Wittfeld, Tony T. Yang, Yuliya Yoncheva, Jendé L. Zijlmans, Martine Hoogman, Barbara Franke, Daan van Rooij, Jan Buitelaar, Christopher R.K. Ching, Ole A. Andreassen, Elena Pozzi, Dick Veltman, Lianne Schmaal, Theo G.M. van Erp, Jessica Turner, F. Xavier Castellanos, Zdenka Pausova, Paul Thompson, Tomas Paus, Pediatric surgery, Anatomy and neurosciences, Psychiatry, Amsterdam Neuroscience - Brain Imaging, Amsterdam Neuroscience - Mood, Anxiety, Psychosis, Stress & Sleep, General Paediatrics, ARD - Amsterdam Reproduction and Development, Paediatrics, Radiology & Nuclear Medicine, Epidemiology, Clinical Cognitive Neuropsychiatry Research Program (CCNP), German Research Foundation, University of Münster, National Health and Medical Research Council (Australia), University of Cape Town, National Research Foundation (South Africa), Swinburne Universit, Jack Brockhoff Foundation, University of Melbourne, Barbara Dicker Brain Sciences Foundation, Rebecca L. Cooper Foundation, Society of Mental Health Research, Swedish Research Council, Swedish Foundation for Strategic Research, Swedish Brain Foundation, Health Research Board (Ireland), Russian Foundation for Basic Research, University of Zurich, Pratt Foundation, Ramsay Health Care, Viertel Charitable Foundation, Schizophrenia Research Institute, European Commission, Australian Research Council, Instituto de Salud Carlos III, National Institute for Health and Care Research (US), National Institute for Health Research (UK), Ministry of Health of the Czech Republic, Bill & Melinda Gates Foundation, South African Medical Research Council, Carnegie Corporation of New York, Wellcome Trust, Medical Research Council (UK), Medical Research Scotland, Netherlands Organization for Scientific Research, Ambrogi, Sonia, Banaschewski, Tobias, Bandeira, Cibele Edom, Cupertino, Renata, Calderoni, Sara, Cannon, Dara, Carr, Vaughan, Chew, Qian Hui, Coghill, David, Cullen, Kathryn, Dahl, Andreas, Epstein, Jeffery, Foran, William, Fortea, Lydia, Fuentes-Claramonte, Paola, Fullerton, Janice M., Furlong, Lisa, Gallagher, Louise, Gao, Si, Gotlib, Ian, Haavik, Jan, Henskens, Frans, Hilland, Eva, Hoekstra, Pieter J, Howells, Fleur M, Ipser, Jonathan, Jørgensen, Jes Kristian, Karantonis, James A., Lawrie, Stephen, Research Institute of the Hospital for Sick Children and University of Toronto, University of Toronto, Departments of Physiology and Nutritional Sciences, University of Toronto, Toronto, Canada, KG Jebsen Centre for Psychosis Research, University of Oslo (UiO)-Institute of Clinical Medicine-Oslo University Hospital [Oslo], Universidad Complutense de Madrid = Complutense University of Madrid [Madrid] (UCM), Mental Health Sciences Unit, University College of London [London] (UCL), Institut de Neurosciences de la Timone (INT), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS), Clinical and Behavioral Neurology - Neuroscienze e riabilitazione, IRCCS Fondazione Santa Lucia [Roma], Heidelberg University, Universidade Federal do Rio Grande do Sul [Porto Alegre] (UFRGS), Universität Heidelberg [Heidelberg] = Heidelberg University, Clinical Neuropsychology, IBBA, APH - Mental Health, Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Hospital Sant Joan de Déu [Barcelona], and Centro de Investigación Biomédica en Red Salud Mental [Madrid] (CIBER-SAM)
Subjects: Bipolar Disorder, Autism Spectrum Disorder, [SDV]Life Sciences [q-bio], Neurogenesis, pathology [Premature Birth], Neurodevelopment, Cortical surface area, pathology [Autism Spectrum Disorder], Cortical growth, methods [Magnetic Resonance Imaging], SDG 3 - Good Health and Well-being, Pregnancy, 130 000 Cognitive Neurology & Memory, Humans, ddc:610, Child, Biological Psychiatry, Cerebral Cortex, pathology [Depressive Disorder, Major], Depressive Disorder, Major, Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], Infant, Newborn, Magnetic Resonance Imaging, Mental illness, Attention Deficit Disorder with Hyperactivity, Premature Birth, genetics [Autism Spectrum Disorder], Female, Psychiatric disorders, 170 000 Motivational & Cognitive Control
Abstract: [Background]: Morphology of the human cerebral cortex differs across psychiatric disorders, with neurobiology and developmental origins mostly undetermined. Deviations in the tangential growth of the cerebral cortex during pre/perinatal periods may be reflected in individual variations in cortical surface area later in life., [Methods]: Interregional profiles of group differences in surface area between cases and controls were generated using T1-weighted magnetic resonance imaging from 27,359 individuals including those with attention-deficit/hyperactivity disorder, autism spectrum disorder, bipolar disorder, major depressive disorder, schizophrenia, and high general psychopathology (through the Child Behavior Checklist). Similarity of interregional profiles of group differences in surface area and prenatal cell-specific gene expression was assessed., [Results]: Across the 11 cortical regions, group differences in cortical area for attention-deficit/hyperactivity disorder, schizophrenia, and Child Behavior Checklist were dominant in multimodal association cortices. The same interregional profiles were also associated with interregional profiles of (prenatal) gene expression specific to proliferative cells, namely radial glia and intermediate progenitor cells (greater expression, larger difference), as well as differentiated cells, namely excitatory neurons and endothelial and mural cells (greater expression, smaller difference). Finally, these cell types were implicated in known pre/perinatal risk factors for psychosis. Genes coexpressed with radial glia were enriched with genes implicated in congenital abnormalities, birth weight, hypoxia, and starvation. Genes coexpressed with endothelial and mural genes were enriched with genes associated with maternal hypertension and preterm birth., [Conclusions]: Our findings support a neurodevelopmental model of vulnerability to mental illness whereby prenatal risk factors acting through cell-specific processes lead to deviations from typical brain development during pregnancy., This work was supported by the German Research Foundation (DFG Grant Nos. HA7070/2-2, HA7070/3, HA7070/4 [to TH]) and IZKF of the medical faculty of Münster (Grants No. Dan3/012/17 [to UD] and MzH 3/020/20 [to TH]), and NHMRC projects (Grant No. 1064643 [to BJH] and 1024570 [to CGD]). The CIAM study was supported by the University of Cape Town Research Committee, South African National Research Foundation, and the South African Medical Research Council (principal investigator [PI], Fleur M. Howells) and Grant No. R01MH117601 (to NJ). This work was funded by the German Research Foundation (Grant Nos. FOR2107 JA 1890/7-1 and FOR2107 JA 1890/7-2 [to AJ]) and Swinburne University scholarship/Australian Postgraduate Award (to JK). Collection of the COGSBD cohort was funded by the Jack Brockhoff Foundation, University of Melbourne, Barbara Dicker Brain Sciences Foundation, Rebecca L Cooper Foundation, and the Society of Mental Health Research (to JK). This work was funded by the German Research Foundation (Grant Nos. FOR2107 KI588/14-1 and FOR2107 KI588/14-2 [to TK]). The St. Göran study was supported by grants from the Swedish Research Council (Grant No. 2018-02653 [to ML]), the Swedish foundation for Strategic Research (Grant No. KF10-0039 [to ML]), the Swedish Brain foundation (Grant No. FO2020-0261 [to ML]), and the Swedish Government under the LUA/ALF agreement (Grant Nos. ALF 20170019 and ALFGBG-716801 [to ML]). This work was supported by RFBR (Grant No. 20-013-00748 [to IL, AST]) and funded by the Health Research Board (Grant No. HRA_POR/2011/100 [to CM]). The Australian Schizophrenia Research Bank (ASRB) was supported by the NHMRC (Enabling Grant No. 386500), the Pratt Foundation, Ramsay Health Care, the Viertel Charitable Foundation, and the Schizophrenia Research Institute. Chief investigators for ASRB were VC, US, RSc, AJ, BM, PTM, SVC, FH, and CPa. This work was supported by Deutsche Forschungsgemeinschaft (Grant Nos. DFG NE 2254/2-1, NE 2254/3-1, NE2254/4-1 [to IN]), the University Research Priority Program “Integrative Human Physiology” at the University of Zurich (to ROT), an NHMRC Senior Principal Research Fellowship (Grant No. 1105825 [to CPa]), an NHMRC L3 Investigator Grant (Grant No. 1196508 [to CPa]), and NHMRC Program Grant (Grant No. 1150083 [to CPa]). ASRB was supported by the NHMRC (Enabling Grant No. 386500), the Pratt Foundation, Ramsay Health Care, the Viertel Charitable Foundation and the Schizophrenia Research Institute. Chief investigators for ASRB were VC, US, RSc, AJ, BM, PTM, SVC, FH, and CPa. This project has received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant (Agreement No. 798181 [to GP]). ASRB was supported by the NHMRC (Enabling Grant, ID 386500), the Pratt Foundation, Ramsay Health Care, the Viertel Charitable Foundation and the Schizophrenia Research Institute. Chief investigators for ASRB were VC, US, RSc, AJ, BM, PTM, SVC, FH, and CPa. The Imaging Genetics in Psychosis study was funded by Project Grants from the NHMRC (Grant Nos. APP630471 and APP1081603 [to YQ]) and the Macquarie University’s Australian Research Council (ARC) Centre of Excellence in Cognition and its Disorders (Grant No. CE110001021 [to YQ]). This work was supported by the Spanish Ministry of Science, Innovation and Universities/Economy and Competitiveness/Instituto de Salud Carlos III (Grant Nos. PI11/01766 and CPII19/00009 [to JR]), co-financed by European Regional Development Fund funds from the European Commission (“A Way of Making Europe”). ASRB was supported by the NHMRC (Enabling Grant No. 386500), the Pratt Foundation, Ramsay Health Care, the Viertel Charitable Foundation, and the Schizophrenia Research Institute. Chief investigators for ASRB were VC, US, RSc, AJ, BM, PTM, SVC, FH, and CPa. SR was supported by an NHMRC Senior Fellowship (Grant No. GNT1154651). Collection of the COGSBD cohort was funded by the Jack Brockhoff Foundation, University of Melbourne, Barbara Dicker Brain Sciences Foundation, Rebecca L Cooper Foundation, and the Society of Mental Health Research (to SR). This work was supported by NIHR; MRC (to KR), NIH (Grant Nos. MH-094268, MH-105660, and MH-107730 [to ASS]). The Neuroimaging of the Children's Attention Project cohort was funded by NHMRC, Australia (Grant No. 1065895). Earlier funding for the cohort as also provided by NHMRC (Grant No. 1008522) and a grant from the Collier Foundation. The ACPU cohort was funded by NHMRC, Australia (Project Grant Nos. 384419 and 569533 [to TS]). This work was supported by research grants from the National Healthcare Group, Singapore (Grant Nos. SIG/05004, SIG/05028, and SIG /1103), and the Singapore Bioimaging Consortium (RP C009/2006 [to KS]), and the Ministry of Health, Czech Republic - conceptual development of research organization (“Institute for Clinical and Experimental Medicine - IKEM, IN 00023001” [to ASk]). This study was supported by the Italian Ministry of Health (Grant No. RC/17-18-19-20-21/A [to GS]) and Ministry of Health of the Czech Republic (Grant No. NU20-04-00393 [to FS]). The Drakenstein Child Health Study (DCHS) cohort is funded by the Bill and Melinda Gates Foundation (Grant No. OPP 1017641) and the South African Medical Research Council. This DCHS contribution was made possible in part by a grant from Carnegie Corporation of New York. The statements made and views expressed are solely the responsibility of the author (DJS). STRADL study was supported and funded by the Wellcome Trust Strategic Award “Stratifying Resilience and Depression Longitudinally” (Grant No. 104036/Z/14/Z), and the Medical Research Council Mental Health Pathfinder Award “Leveraging routinely collected and linked research data to study the causes and consequences of common mental disorders” (MRC, Grant No. MC_PC_17209). Scottish Bipolar Family Study (SBFS) was supported by National Health Service Research Scotland, through the Scottish Mental Health Research Network (www.smhrn.org.uk), who provided assistance with subject recruitment and assessments. SBFS was conducted at the Brain Research Imaging Centre (http://www.bric.ed.ac.uk), which is supported by SINAPSE (Scottish Imaging Network, a Platform for Scientific Excellence, http://www.sinapse.ac.uk). Processing of the datasets used the resources provided by the Edinburgh Compute and Data Facility (http://www.ecdf.ed.ac.uk/) (ASt). TVR was supported by an NHMRC Early Career Fellowship (Grant No. GNT1088785). Collection of the COGSBD cohort was funded by the Jack Brockhoff Foundation, University of Melbourne, Barbara Dicker Brain Sciences Foundation, Rebecca L Cooper Foundation, and the Society of Mental Health Research (to TVR). EV was supported by the Spanish Ministry of Science and Innovation (PI18/00805) integrated into the Plan Nacional de I+D+I and co-financed by the ISCIII-Subdirección General de Evaluación and the FEDER; the Instituto de Salud Carlos III; the CIBERSAM (Centro de Investigación Biomédica en Red de Salud Mental); by the CERCA Programme/Generalitat de Catalunya and the Secretaria d’Universitats i Recerca del Departament d’Economia I Coneixement (Grant No. 2017SGR1355). This study was also supported by the Departament de Salut de la Generalitat de Catalunya, Pla Estratègic de Recerca i Innovació en Salut (PERIS) 2016-2020 (Grant No. SLT006/17/00345) and the European Union Horizon 2020 research and innovation program (EU.3.1.1. Understanding health, wellbeing and disease: Grant Nos. 754907 and EU.3.1.3 [to EB]; Treating and managing disease: Grant No. 945151 [to EV]). This study was supported by the National Center for Complementary and Integrative Health (Grant Nos. R21AT009173 and R61AT009864 [to TTY]); by the National Center for Advancing Translational Sciences (CTSI), National Institutes of Health, through UCSF-CTSI (Grant No. UL1TR001872 [to TTY]); by the American Foundation for Suicide Prevention (Grant No. SRG-1-141-18 [to TTY]); by UCSF Research Evaluation and Allocation Committee (REAC) and J. Jacobson Fund (to TTY); by the NIMH (Grant No. R01MH085734 [to TTY]); and by the Brain and Behavior Research Foundation (formerly NARSAD) (to TTY). This work was supported by a personal Veni grant to MH from the Netherlands Organization for Scientific Research (NWO, Grant No. 91619115 [to MH]) and European Community’s Horizon 2020 Programme (H2020/2014 – 2020) (Grant Agreements Nos. 667302 [CoCA], 728018 [Eat2beNICE], and 847879 [PRIME] [to BF]). JBu has been supported by the EU-AIMS (European Autism Interventions) and AIMS-2-TRIALS programmes, which receive support from Innovative Medicines Initiative Joint Undertaking Grant Nos. 115300 and 777394, the resources of which are composed of financial contributions from the European Union’s FP7 and Horizon 2020 Programmes, and from the European Federation of Pharmaceutical Industries and Associations companies’ in-kind contributions, and AUTISM SPEAKS, Autistica and SFARI; and by the Horizon 2020–supported programme CANDY (Grant No. 847818 [to JBu]). This work is supported by Grant No. NIA T32AG058507 and NIH Grant No. U54EB020403 from the Big Data to Knowledge (BD2K) Program (to CRKC). ENIGMA MDD work is supported by NIH (Grant Nos. U54 EB020403 [to PT], R01 MH116147 [to PT], and R01 MH117601 [to NJ and LS]). LS was supported by an NHMRC Career Development Fellowship (Grant No. 1140764). This work was supported by the National Center for Research Resources at the NIH (Grant Nos. NIH 1 U24 RR021992 [Function Biomedical Informatics Research Network], NIH 1 U24 RR025736-01 [Biomedical Informatics Research Network Coordinating Center; http://www.birncommunity.org]). TGMvE is supported by ENIGMA’s NIH BD2K initiative (Grant No. U54 EB020403), ENIGMA Sex Differences (Grant No. R01MH116147), and ENIGMA-COINSTAC: Advanced Worldwide Transdiagnostic Analysis of Valence System Brain Circuits (Grant No. R01MH121246). This work was supported by the NIH (Grant No. R01MH121246 [to JT, Calhoun, and TGMvE]). This work was supported in part by NIH (Grant No. U54 EB020403 [to PT]).
Published: 2022
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4. Attention-deficit/hyperactivity disorder and brain metabolites from proton magnetic resonance spectroscopy: a systematic review and meta-analysis protocol

Author: Marcos Vinícius Vidor, Cibele Edom Bandeira, Eugenio H. Grevet, Alexandre Ribeiro Martins, Diego L. Rovaris, Claiton H.D. Bau, Renata B. Cupertino, Luis Augusto Rohde, and Alana Castro Panzenhagen
Subjects: MRS, spectroscopy, Proton Magnetic Resonance Spectroscopy, RC435-571, Review Article, 03 medical and health sciences, Metanálise, 0302 clinical medicine, Meta-Analysis as Topic, medicine, Attention deficit hyperactivity disorder, ADHD, Humans, 0501 psychology and cognitive sciences, Neurochemistry, protocol, Protocol (science), Psychiatry, Metabolismo, Espectroscopia de prótons por ressonância magnética, medicine.diagnostic_test, business.industry, 05 social sciences, Brain, General Medicine, Transtorno do déficit de atenção com hiperatividade, medicine.disease, Magnetic Resonance Imaging, Proton magnetic resonance, 030227 psychiatry, meta-analysis, Psychiatry and Mental health, Systematic review, Revisão sistemática, Attention Deficit Disorder with Hyperactivity, Meta-analysis, Functional magnetic resonance imaging, business, Neuroscience, 050104 developmental & child psychology, Cérebro, Systematic Reviews as Topic
Abstract: Despite major advances in the study of the brain, investigations on neurochemistry in vivo still lack the solid ground of more established methods, such as structural and functional magnetic resonance imaging. Proton magnetic resonance spectroscopy (MRS) is a technique that might potentially fill in this gap. Nevertheless, studies using this approach feature great methodological heterogeneity, such as varying voxel of choice, differences on emphasized metabolites, and absence of a standardized unit. In this study, we present a methodology for creating a systematic review and meta-analysis for this kind of scientific evidence using the prototypical case of attention-deficit/hyperactivity disorder. Systematic review registration: International Prospective Register of Systematic Reviews (PROSPERO), CRD42018112418.
Published: 2021

5. T1. THE SHARED BIOLOGY BETWEEN THE GROWTH HORMONE (GH)–INSULIN-LIKE GROWTH FACTOR (IGF)-I AXIS, NEURODEVELOPMENTAL AND RELATED NEUROPSYCHIATRIC DISORDERS

Author: Isabela C. Velloso-Oliveira, Iago Junger-Santos, Leonardo Marchetti, Clara S. Gusmão, Eugênio H. Grevet, Claiton H.D. Bau, Bruna Santos da Silva, and Diego Luiz Rovaris
Subjects: Pharmacology, Psychiatry and Mental health, Neurology, Pharmacology (medical), Neurology (clinical), Biological Psychiatry
Published: 2022
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6. Oxidative damage, inflammation, genotoxic effect, and global DNA methylation caused by inhalation of formaldehyde and the purpose of melatonin

Author: Claiton H.D. Bau, Marina de Souza Vencato, Diana Müller, Letícia Bernardini, Natália Brucker, Eduardo Barbosa, Carolina S Stein, Gabriela Göethel, Solange Cristina Garcia, Rafael Noal Moresco, Mariele Feiffer Charão, and Nadine Arnold Steffens
Subjects: Paper, 0303 health sciences, medicine.medical_specialty, DNA damage, Chemistry, Health, Toxicology and Mutagenesis, 010501 environmental sciences, Toxicology, medicine.disease_cause, 01 natural sciences, Melatonin, Comet assay, Lipid peroxidation, 03 medical and health sciences, chemistry.chemical_compound, Endocrinology, Internal medicine, Micronucleus test, TBARS, medicine, Genotoxicity, Oxidative stress, 030304 developmental biology, 0105 earth and related environmental sciences, medicine.drug
Abstract: Formaldehyde (FA) exposure has been proven to increase the risk of asthma and cancer. This study aimed to evaluate for 28 days the FA inhalation effects on oxidative stress, inflammation process, genotoxicity, and global DNA methylation in mice as well as to investigate the potential protective effects of melatonin. For that, analyses were performed on lung, liver and kidney tissues, blood, and bone marrow. Bronchoalveolar lavage was used to measure inflammatory parameters. Lipid peroxidation (TBARS), protein carbonyl (PCO), non-protein thiols (NPSH), catalase activity (CAT), comet assay, micronuclei (MN), and global methylation were determined. The exposure to 5-ppm FA resulted in oxidative damage to the lung, presenting a significant increase in TBARS and NO levels and a decrease in NPSH levels, besides an increase in inflammatory cells recruited for bronchoalveolar lavage. Likewise, in the liver tissue, the exposure to 5-ppm FA increased TBARS and PCO levels and decreased NPSH levels. In addition, FA significantly induced DNA damage, evidenced by the increase of % tail moment and MN frequency. The pretreatment of mice exposed to FA applying melatonin improved inflammatory and oxidative damage in lung and liver tissues and attenuated MN formation in bone marrow cells. The pulmonary histological study reinforced the results observed in biochemical parameters, demonstrating the potential beneficial role of melatonin. Therefore, our results demonstrated that FA exposure with repeated doses might induce oxidative damage, inflammatory, and genotoxic effects, and melatonin minimized the toxic effects caused by FA inhalation in mice.
Published: 2020
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7. The neuroendocrine modulation of global DNA methylation in neuropsychiatric disorders

Author: Diego L. Rovaris, Claiton H.D. Bau, Mariele Feiffer Charão, Bruna Santos da Silva, Diana Müller, and Eugenio H. Grevet
Subjects: 0301 basic medicine, education, Biology, Bioinformatics, Environmental stress, Mental health, Sexual hormones, 03 medical and health sciences, Cellular and Molecular Neuroscience, Psychiatry and Mental health, 030104 developmental biology, 0302 clinical medicine, DNA methylation, Molecular Biology, 030217 neurology & neurosurgery, Hormone
Abstract: There is an increasing body of knowledge on the influence of differential DNA methylation of specific genomic regions in psychiatric disorders. However, fewer studies have addressed global DNA methylation (GMe) levels. GMe is an estimative of biological functioning that is regulated by pervasive mechanisms able to capture the big picture of metabolic and environmental influences upon gene expression. In the present perspective article, we highlighted evidence for the relationships between cortisol and sex hormones and GMe in psychiatric disorders. We argue that the far-reaching effects of cortisol and sexual hormones on GMe may lie on the pathways linking stress and mental health. Further research on these endocrine-epigenetic links may help to explain the role of environmental stress as well as sex differences in the prevalence of psychiatric disorders.
Published: 2020
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8. Association of CHRNA5 Gene Variants with Crack Cocaine Addiction

Author: Angelita P. Aroche, Anderson Ravy Stolf, Claiton H.D. Bau, Jaqueline Bohrer Schuch, Lisia von Diemen, Diego L. Rovaris, Breno Sanvicente-Vieira, Felix Kessler, Eugenio H. Grevet, and Rodrigo Grassi-Oliveira
Subjects: Adult, Male, Risk, 0301 basic medicine, Genotype, media_common.quotation_subject, Nerve Tissue Proteins, Genome-wide association study, Single-nucleotide polymorphism, Receptors, Nicotinic, Bioinformatics, Polymorphism, Single Nucleotide, Nicotine, Cocaine-Related Disorders, Structure-Activity Relationship, Young Adult, 03 medical and health sciences, Cellular and Molecular Neuroscience, 0302 clinical medicine, mental disorders, Humans, Medicine, Computer Simulation, Genetic Predisposition to Disease, Allele, Alleles, media_common, biology, business.industry, Addiction, CHRNA5, Haplotype, medicine.disease, Substance abuse, 030104 developmental biology, Haplotypes, Neurology, Case-Control Studies, biology.protein, Crack Cocaine, Molecular Medicine, Female, business, 030217 neurology & neurosurgery, Genome-Wide Association Study, medicine.drug
Abstract: Genome-wide studies provide increasing evidence of association of genetic variants with different behaviors. However, there is a growing need for replication and subsequent characterization of specific findings. In this sense, the CHRNA5 gene has been associated with nicotine (with genome-wide significance), alcohol and cocaine addictions. So far, this gene has not been evaluated in smoked (crack) cocaine. We aimed to analyze the influence of CHRNA5 variants in crack addiction susceptibility and severity. The sample includes 300 crack-addicted patients and 769 non-addicted individuals. The CHRNA5 SNPs evaluated were rs588765, rs16969968, and rs514743. Homozygosity for rs16969968 and rs588765 major alleles was nominally associated with a risk to crack addiction (GG, P = 0.032; CC, P = 0.036, respectively). Haplotype analyses reveal significant associations (rs588765|rs16969968|rs514743 pglobal-corrected = 7.66 × 10–5) and suggest a substantial role for rs16969968. These findings corroborate previous reports in cocaine addiction—in line with the expected effects of cocaine in the cholinergic system—and in the opposite direction of significant GWAS findings for nicotine addiction susceptibility. These results are strengthened by the first report of an association of rs588765 with crack addiction and by the haplotype findings. In summary, our study highlights the relevance of the α5 subunit on crack cocaine addiction, replicating previous results relating CHRNA5 with the genetics and pathophysiology of addiction of different drugs.
Published: 2020
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9. Meta-analysis and systematic review of ADGRL3 (LPHN3) polymorphisms in ADHD susceptibility

Author: Marieke Klein, Claiton H.D. Bau, Paula Rovira, Thomas P. Quinn, Barbara Franke, Carlos Renato Moreira-Maia, Nina Roth Mota, Djenifer B. Kappel, Mauricio Arcos-Burgos, Cristina Sánchez-Mora, Eugenio H. Grevet, Luis Augusto Rohde, Mara H. Hutz, M. Ribasés, Glaucia Chiyoko Akutagava-Martins, and Estela M. Bruxel
Subjects: 0301 basic medicine, Oncology, medicine.medical_specialty, Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], business.industry, Genome-wide association study, Single-nucleotide polymorphism, medicine.disease, Gene association, 03 medical and health sciences, Cellular and Molecular Neuroscience, Psychiatry and Mental health, 030104 developmental biology, 0302 clinical medicine, Internal medicine, Meta-analysis, medicine, Latrophilin 3, Attention deficit hyperactivity disorder, Allele, business, Molecular Biology, 030217 neurology & neurosurgery, Genetic association
Abstract: Contains fulltext : 237889.pdf (Publisher’s version ) (Open Access) The gene encoding adhesion G protein-coupled receptor L3 (ADGRL3, also referred to as latrophilin 3 or LPHN3) has been associated with ADHD susceptibility in independent ADHD samples. We conducted a systematic review and a comprehensive meta-analysis to summarize the associations between the most studied ADGRL3 polymorphisms (rs6551665, rs1947274, rs1947275, and rs2345039) and both childhood and adulthood ADHD. Eight association studies (seven published and one unpublished) fulfilled criteria for inclusion in our meta-analysis. We also incorporated GWAS data for ADGRL3. In order to avoid overlapping samples, we started with summary statistics from GWAS samples and then added data from gene association studies. The results of our meta-analysis suggest an effect of ADGRL3 variants on ADHD susceptibility in children (n = 8724/14,644 cases/controls and 1893 families): rs6551665 A allele (Z score = -2.701; p = 0.0069); rs1947274 A allele (Z score = -2.033; p = 0.0421); rs1947275 T allele (Z score = 2.339; p = 0.0978); and rs2345039 C allele (Z score = 3.806; p = 0.0026). Heterogeneity was found in analyses for three SNPs (rs6551665, rs1947274, and rs2345039). In adults, results were not significant (n = 6532 cases/15,874 controls): rs6551665 A allele (Z score = 2.005; p = 0.0450); rs1947274 A allele (Z score = 2.179; p = 0.0293); rs1947275 T allele (Z score = -0.822; p = 0.4109); and rs2345039 C allele (Z score = -1.544; p = 0.1226). Heterogeneity was found just for rs6551665. In addition, funnel plots did not suggest publication biases. Consistent with ADGRL3's role in early neurodevelopment, our findings suggest that the gene is predominantly associated with childhood ADHD.
Published: 2020
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10. Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

Author: Niamh Mullins, JooEun Kang, Adrian I. Campos, Jonathan R.I. Coleman, Alexis C. Edwards, Hanga Galfalvy, Daniel F. Levey, Adriana Lori, Andrey Shabalin, Anna Starnawska, Mei-Hsin Su, Hunna J. Watson, Mark Adams, Swapnil Awasthi, Michael Gandal, Jonathan D. Hafferty, Akitoyo Hishimoto, Minsoo Kim, Satoshi Okazaki, Ikuo Otsuka, Stephan Ripke, Erin B. Ware, Andrew W. Bergen, Wade H. Berrettini, Martin Bohus, Harry Brandt, Xiao Chang, Wei J. Chen, Hsi-Chung Chen, Steven Crawford, Scott Crow, Emily DiBlasi, Philibert Duriez, Fernando Fernández-Aranda, Manfred M. Fichter, Steven Gallinger, Stephen J. Glatt, Philip Gorwood, Yiran Guo, Hakon Hakonarson, Katherine A. Halmi, Hai-Gwo Hwu, Sonia Jain, Stéphane Jamain, Susana Jiménez-Murcia, Craig Johnson, Allan S. Kaplan, Walter H. Kaye, Pamela K. Keel, James L. Kennedy, Kelly L. Klump, Dong Li, Shih-Cheng Liao, Klaus Lieb, Lisa Lilenfeld, Chih-Min Liu, Pierre J. Magistretti, Christian R. Marshall, James E. Mitchell, Eric T. Monson, Richard M. Myers, Dalila Pinto, Abigail Powers, Nicolas Ramoz, Stefan Roepke, Vsevolod Rozanov, Stephen W. Scherer, Christian Schmahl, Marcus Sokolowski, Michael Strober, Laura M. Thornton, Janet Treasure, Ming T. Tsuang, Stephanie H. Witt, D. Blake Woodside, Zeynep Yilmaz, Lea Zillich, Rolf Adolfsson, Ingrid Agartz, Tracy M. Air, Martin Alda, Lars Alfredsson, Ole A. Andreassen, Adebayo Anjorin, Vivek Appadurai, María Soler Artigas, Sandra Van der Auwera, M. Helena Azevedo, Nicholas Bass, Claiton H.D. Bau, Bernhard T. Baune, Frank Bellivier, Klaus Berger, Joanna M. Biernacka, Tim B. Bigdeli, Elisabeth B. Binder, Michael Boehnke, Marco P. Boks, Rosa Bosch, David L. Braff, Richard Bryant, Monika Budde, Enda M. Byrne, Wiepke Cahn, Miguel Casas, Enrique Castelao, Jorge A. Cervilla, Boris Chaumette, Sven Cichon, Aiden Corvin, Nicholas Craddock, David Craig, Franziska Degenhardt, Srdjan Djurovic, Howard J. Edenberg, Ayman H. Fanous, Jerome C. Foo, Andreas J. Forstner, Mark Frye, Janice M. Fullerton, Justine M. Gatt, Pablo V. Gejman, Ina Giegling, Hans J. Grabe, Melissa J. Green, Eugenio H. Grevet, Maria Grigoroiu-Serbanescu, Blanca Gutierrez, Jose Guzman-Parra, Steven P. Hamilton, Marian L. Hamshere, Annette Hartmann, Joanna Hauser, Stefanie Heilmann-Heimbach, Per Hoffmann, Marcus Ising, Ian Jones, Lisa A. Jones, Lina Jonsson, René S. Kahn, John R. Kelsoe, Kenneth S. Kendler, Stefan Kloiber, Karestan C. Koenen, Manolis Kogevinas, Bettina Konte, Marie-Odile Krebs, Mikael Landén, Jacob Lawrence, Marion Leboyer, Phil H. Lee, Douglas F. Levinson, Calwing Liao, Jolanta Lissowska, Susanne Lucae, Fermin Mayoral, Susan L. McElroy, Patrick McGrath, Peter McGuffin, Andrew McQuillin, Sarah E. Medland, Divya Mehta, Ingrid Melle, Yuri Milaneschi, Philip B. Mitchell, Esther Molina, Gunnar Morken, Preben Bo Mortensen, Bertram Müller-Myhsok, Caroline Nievergelt, Vishwajit Nimgaonkar, Markus M. Nöthen, Michael C. O’Donovan, Roel A. Ophoff, Michael J. Owen, Carlos Pato, Michele T. Pato, Brenda W.J.H. Penninx, Jonathan Pimm, Giorgio Pistis, James B. Potash, Robert A. Power, Martin Preisig, Digby Quested, Josep Antoni Ramos-Quiroga, Andreas Reif, Marta Ribasés, Vanesa Richarte, Marcella Rietschel, Margarita Rivera, Andrea Roberts, Gloria Roberts, Guy A. Rouleau, Diego L. Rovaris, Dan Rujescu, Cristina Sánchez-Mora, Alan R. Sanders, Peter R. Schofield, Thomas G. Schulze, Laura J. Scott, Alessandro Serretti, Jianxin Shi, Stanley I. Shyn, Lea Sirignano, Pamela Sklar, Olav B. Smeland, Jordan W. Smoller, Edmund J.S. Sonuga-Barke, Gianfranco Spalletta, John S. Strauss, Beata Świątkowska, Maciej Trzaskowski, Gustavo Turecki, Laura Vilar-Ribó, John B. Vincent, Henry Völzke, James T.R. Walters, Cynthia Shannon Weickert, Thomas W. Weickert, Myrna M. Weissman, Leanne M. Williams, Naomi R. Wray, Clement C. Zai, Allison E. Ashley-Koch, Jean C. Beckham, Elizabeth R. Hauser, Michael A. Hauser, Nathan A. Kimbrel, Jennifer H. Lindquist, Benjamin McMahon, David W. Oslin, Xuejun Qin, Esben Agerbo, Anders D. Børglum, Gerome Breen, Annette Erlangsen, Tõnu Esko, Joel Gelernter, David M. Hougaard, Ronald C. Kessler, Henry R. Kranzler, Qingqin S. Li, Nicholas G. Martin, Andrew M. McIntosh, Ole Mors, Merete Nordentoft, Catherine M. Olsen, David Porteous, Robert J. Ursano, Danuta Wasserman, Thomas Werge, David C. Whiteman, Cynthia M. Bulik, Hilary Coon, Ditte Demontis, Anna R. Docherty, Po-Hsiu Kuo, Cathryn M. Lewis, J. John Mann, Miguel E. Rentería, Daniel J. Smith, Eli A. Stahl, Murray B. Stein, Fabian Streit, Virginia Willour, Douglas M. Ruderfer, Manuel Mattheisen, Abdel Abdellaoui, Mark J. Adams, Till F.M. Andlauer, Silviu-Alin Bacanu, Marie Bækvad-Hansen, Aartjan T.F. Beekman, Julien Bryois, Henriette N. Buttenschøn, Jonas Bybjerg-Grauholm, Na Cai, Jane Hvarregaard Christensen, Toni-Kim Clarke, Lucía Colodro-Conde, Baptiste Couvy-Duchesne, Nick Craddock, Gregory E. Crawford, Gail Davies, Eske M. Derks, Nese Direk, Conor V. Dolan, Erin C. Dunn, Thalia C. Eley, Valentina Escott-Price, Farnush Farhadi Hassan Kiadeh, Hilary K. Finucane, Josef Frank, Héléna A. Gaspar, Michael Gill, Fernando S. Goes, Scott D. Gordon, Shantel Marie Weinsheimer, Jürgen Wellmann, Gonneke Willemsen, Yang Wu, Hualin S. Xi, Jian Yang, Futao Zhang, Volker Arolt, Dorret I. Boomsma, Udo Dannlowski, E.J.C. de Geus, J. Raymond Depaulo, Enrico Domenici, Katharina Domschke, Jakob Grove, Lynsey S. Hall, Christine Søholm Hansen, Thomas F. Hansen, Stefan Herms, Ian B. Hickie, Georg Homuth, Carsten Horn, Jouke-Jan Hottenga, David M. Howard, Rick Jansen, Eric Jorgenson, James A. Knowles, Isaac S. Kohane, Julia Kraft, Warren W. Kretzschmar, Zoltán Kutalik, Yihan Li, Penelope A. Lind, Donald J. MacIntyre, Dean F. MacKinnon, Robert M. Maier, Wolfgang Maier, Jonathan Marchini, Hamdi Mbarek, Christel M. Middeldorp, Evelin Mihailov, Lili Milani, Francis M. Mondimore, Grant W. Montgomery, Sara Mostafavi, Matthias Nauck, Bernard Ng, Michel G. Nivard, Dale R. Nyholt, Paul F. O’Reilly, Hogni Oskarsson, Caroline Hayward, Andrew C. Heath, Glyn Lewis, Pamela A.F. Madden, Patrik K. Magnusson, Andres Metspalu, Sara A. Paciga, Nancy L. Pedersen, Jodie N. Painter, Carsten Bøcker Pedersen, Marianne Giørtz Pedersen, Roseann E. Peterson, Wouter J. Peyrot, Danielle Posthuma, Jorge A. Quiroz, Per Qvist, John P. Rice, Brien P. Riley, Saira Saeed Mirza, Robert Schoevers, Eva C. Schulte, Ling Shen, Engilbert Sigurdsson, Grant C.B. Sinnamon, Johannes H. Smit, Hreinn Stefansson, Stacy Steinberg, Jana Strohmaier, Katherine E. Tansey, Henning Teismann, Alexander Teumer, Wesley Thompson, Pippa A. Thomson, Thorgeir E. Thorgeirsson, Matthew Traylor, Jens Treutlein, Vassily Trubetskoy, André G. Uitterlinden, Daniel Umbricht, Albert M. van Hemert, Alexander Viktorin, Peter M. Visscher, Yunpeng Wang, Bradley T. Webb, Roy H. Perlis, David J. Porteous, Catherine Schaefer, Kari Stefansson, Henning Tiemeier, Rudolf Uher, Patrick F. Sullivan, Kevin S. O’Connell, Brandon Coombes, Zhen Qiao, Thomas D. Als, Sigrid Børte, Alexander W. Charney, Ole Kristian Drange, Michael J. Gandal, Saskia P. Hagenaars, Masashi Ikeda, Nolan Kamitaki, Kristi Krebs, Georgia Panagiotaropoulou, Brian M. Schilder, Laura G. Sloofman, Bendik S. Winsvold, Hong-Hee Won, Liliya Abramova, Kristina Adorjan, Mariam Al Eissa, Diego Albani, Ney Alliey-Rodriguez, Verneri Antilla, Anastasia Antoniou, Ji Hyun Baek, Michael Bauer, Eva C. Beins, Sarah E. Bergen, Armin Birner, Erlend Bøen, Murielle Brum, Ben M. Brumpton, Nathalie Brunkhorst-Kanaan, William Byerley, Murray Cairns, Miquel Casas, Pablo Cervantes, Cristiana Cruceanu, Alfredo Cuellar-Barboza, Julie Cunningham, David Curtis, Piotr M. Czerski, Anders M. Dale, Nina Dalkner, Friederike S. David, Amanda L. Dobbyn, Athanassios Douzenis, Torbjørn Elvsåshagen, I. Nicol Ferrier, Alessia Fiorentino, Tatiana M. Foroud, Liz Forty, Oleksandr Frei, Nelson B. Freimer, Louise Frisén, Katrin Gade, Julie Garnham, Ian R. Gizer, Katherine Gordon-Smith, Tiffany A. Greenwood, José Guzman-Parra, Kyooseob Ha, Magnus Haraldsson, Martin Hautzinger, Urs Heilbronner, Dennis Hellgren, Peter A. Holmans, Laura Huckins, Jessica S. Johnson, Janos L. Kalman, Yoichiro Kamatani, Sarah Kittel-Schneider, Maria Koromina, Thorsten M. Kranz, Michiaki Kubo, Ralph Kupka, Steven A. Kushner, Catharina Lavebratt, Markus Leber, Heon-Jeong Lee, Shawn E. Levy, Catrin Lewis, Martin Lundberg, Sigurdur H. Magnusson, Adam Maihofer, Dolores Malaspina, Eirini Maratou, Lina Martinsson, Nathaniel W. McGregor, James D. McKay, Helena Medeiros, Vincent Millischer, Jennifer L. Moran, Derek W. Morris, Thomas W. Mühleisen, Niamh O’Brien, Claire O’Donovan, Loes M. Olde Loohuis, Lilijana Oruc, Sergi Papiol, Antonio F. Pardiñas, Amy Perry, Andrea Pfennig, Evgenia Porichi, Towfique Raj, Mark H. Rapaport, J. Raymond DePaulo, Eline J. Regeer, Fabio Rivas, Julian Roth, Panos Roussos, Fanny Senner, Sally Sharp, Paul D. Shilling, Claire Slaney, Janet L. Sobell, Maria Soler Artigas, Anne T. Spijker, Dan J. Stein, Chikashi Terao, Claudio Toma, Paul Tooney, Evangelia-Eirini Tsermpini, Marquis P. Vawter, Helmut Vedder, Simon Xi, Wei Xu, Jessica Mei Kay Yang, Allan H. Young, Hannah Young, Peter P. Zandi, Hang Zhou, null HUNT All-In Psychiatry, Gulja Babadjanova, Lena Backlund, Susanne Bengesser, Douglas H.R. Blackwood, Vaughan J. Carr, Stanley Catts, Dimitris Dikeos, Bruno Etain, Panagiotis Ferentinos, Micha Gawlik, Elliot S. Gershon, Frans Henskens, Jan Hillert, Kyung Sue Hong, Christina M. Hultman, Kristian Hveem, Nakao Iwata, Assen V. Jablensky, George Kirov, Christine Lochner, Carmel Loughland, Carol A. Mathews, Francis J. McMahon, Patricia Michie, Bryan Mowry, Benjamin M. Neale, Caroline M. Nievergelt, Ketil J. Oedegaard, Tomas Olsson, Chris Pantelis, George P. Patrinos, Eva Z. Reininghaus, Takeo Saito, Ulrich Schall, Martin Schalling, Rodney J. Scott, Eystein Stordal, Arne E. Vaaler, Eduard Vieta, Irwin D. Waldman, John-Anker Zwart, John I. Nurnberger, Arianna Di Florio, Roger A.H. Adan, Tetsuya Ando, Harald Aschauer, Jessica H. Baker, Vladimir Bencko, Andreas Birgegård, Joseph M. Boden, Ilka Boehm, Claudette Boni, Vesna Boraska Perica, Katharina Buehren, Roland Burghardt, Laura Carlberg, Matteo Cassina, Maurizio Clementi, Roger D. Cone, Philippe Courtet, James J. Crowley, Unna N. Danner, Oliver S.P. Davis, Martina de Zwaan, George Dedoussis, Daniela Degortes, Janiece E. DeSocio, Danielle M. Dick, Christian Dina, Monika Dmitrzak-Weglarz, Elisa Docampo Martinez, Laramie E. Duncan, Karin Egberts, Morten Mattingsdal, Sara McDevitt, Ingrid Meulenbelt, Nadia Micali, James Mitchell, Karen Mitchell, Palmiero Monteleone, Alessio Maria Monteleone, Melissa A. Munn-Chernoff, Benedetta Nacmias, Marie Navratilova, Ioanna Ntalla, Julie K. O’Toole, Leonid Padyukov, Aarno Palotie, Jacques Pantel, Hana Papezova, Richard Parker, John F. Pearson, Stefan Ehrlich, Geòrgia Escaramís, Thomas Espeseth, Xavier Estivill, Anne Farmer, Angela Favaro, Krista Fischer, James A.B. Floyd, Manuel Föcker, Lenka Foretova, Monica Forzan, Christopher S. Franklin, Giovanni Gambaro, Johanna Giuranna, Paola Giusti-Rodríquez, Fragiskos Gonidakis, Scott Gordon, Monica Gratacos Mayora, Sébastien Guillaume, Ken B. Hanscombe, Konstantinos Hatzikotoulas, Johannes Hebebrand, Sietske G. Helder, Anjali K. Henders, Beate Herpertz-Dahlmann, Wolfgang Herzog, Anke Hinney, L. John Horwood, Christopher Hübel, Liselotte V. Petersen, Kirstin L. Purves, Anu Raevuori, Ted Reichborn-Kjennerud, Valdo Ricca, Samuli Ripatti, Franziska Ritschel, Marion Roberts, Filip Rybakowski, Paolo Santonastaso, André Scherag, Ulrike Schmidt, Nicholas J. Schork, Alexandra Schosser, Jochen Seitz, Lenka Slachtova, P. Eline Slagboom, Margarita C.T. Slof-Op ‘t Landt, Agnieszka Slopien, Nicole Soranzo, Sandro Sorbi, Lorraine Southam, Vidar W. Steen, Laura M. Huckins, James I. Hudson, Hartmut Imgart, Hidetoshi Inoko, Vladimir Janout, Jennifer Jordan, Antonio Julià, Gursharan Kalsi, Deborah Kaminská, Jaakko Kaprio, Leila Karhunen, Andreas Karwautz, Martien J.H. Kas, Martin A. Kennedy, Anna Keski-Rahkonen, Kirsty Kiezebrink, Youl-Ri Kim, Katherine M. Kirk, Lars Klareskog, Gun Peggy S. Knudsen, Janne T. Larsen, Stephanie Le Hellard, Virpi M. Leppä, Paul Lichtenstein, Bochao Danae Lin, Astri Lundervold, Jurjen Luykx, Mario Maj, Katrin Mannik, Sara Marsal, Garret D. Stuber, Jin P. Szatkiewicz, Ioanna Tachmazidou, Elena Tenconi, Alfonso Tortorella, Federica Tozzi, Artemis Tsitsika, Marta Tyszkiewicz-Nwafor, Konstantinos Tziouvas, Annemarie A. van Elburg, Eric F. van Furth, Tracey D. Wade, Gudrun Wagner, Esther Walton, H. Erich Wichmann, Elisabeth Widen, Shuyang Yao, Eleftheria Zeggini, Stephanie Zerwas, Stephan Zipfel, Martin Jungkunz, Lydie Dietl, Cornelia E. Schwarze, Norbert Dahmen, Björn H. Schott, Arian Mobascher, Silvia Crivelli, Michelle F. Dennis, Phillip D. Harvey, Bruce W. Carter, Jennifer E. Huffman, Daniel Jacobson, Ravi Madduri, Maren K. Olsen, John Pestian, J. Michael Gaziano, Sumitra Muralidhar, Rachel Ramoni, Jean Beckham, Kyong-Mi Chang, Christopher J. O’Donnell, Philip S. Tsao, James Breeling, Grant Huang, J.P. Casas Romero, Jennifer Moser, Stacey B. Whitbourne, Jessica V. Brewer, Mihaela Aslan, Todd Connor, Dean P. Argyres, Brady Stephens, Mary T. Brophy, Donald E. Humphries, Luis E. Selva, Nhan Do, Shahpoor Shayan, Kelly Cho, Saiju Pyarajan, Elizabeth Hauser, Yan Sun, Hongyu Zhao, Peter Wilson, Rachel McArdle, Louis Dellitalia, Kristin Mattocks, John Harley, Clement J. Zablocki, Jeffrey Whittle, Frank Jacono, Salvador Gutierrez, Gretchen Gibson, Kimberly Hammer, Laurence Kaminsky, Gerardo Villareal, Scott Kinlay, Junzhe Xu, Mark Hamner, Roy Mathew, Sujata Bhushan, Pran Iruvanti, Michael Godschalk, Zuhair Ballas, Douglas Ivins, Stephen Mastorides, Jonathan Moorman, Saib Gappy, Jon Klein, Nora Ratcliffe, Hermes Florez, Olaoluwa Okusaga, Maureen Murdoch, Peruvemba Sriram, Shing Shing Yeh, Neeraj Tandon, Darshana Jhala, Samuel Aguayo, David Cohen, Satish Sharma, Suthat Liangpunsakul, Kris Ann Oursler, Mary Whooley, Sunil Ahuja, Joseph Constans, Paul Meyer, Jennifer Greco, Michael Rauchman, Richard Servatius, Melinda Gaddy, Agnes Wallbom, Timothy Morgan, Todd Stapley, Scott Sherman, George Ross, Philip Tsao, Patrick Strollo, Edward Boyko, Laurence Meyer, Samir Gupta, Mostaqul Huq, Joseph Fayad, Adriana Hung, Jack Lichy, Robin Hurley, Brooks Robey, Robert Striker, Dietl, Lydie, Schwarze, Cornelia E., Dahmen, Norbert, Schott, Björn H., Nöthen, Markus M., Ripke, Stephan, Mobascher, Arian, Rujescu, Dan, Lieb, Klaus, Roepke, Stefan, Schmahl, Christian, Bohus, Martin, Rietschel, Marcella, Crivelli, Silvia, Dennis, Michelle F., Harvey, Phillip D., Carter, Bruce W., Huffman, Jennifer E., Jacobson, Daniel, Madduri, Ravi, Olsen, Maren K., Pestian, John, Gaziano, J. Michael, Muralidhar, Sumitra, Ramoni, Rachel, Beckham, Jean, Chang, Kyong-Mi, O'Donnell, Christopher J., Tsao, Philip S., Breeling, James, Huang, Grant, Romero, J. P. Casas, Moser, Jennifer, Whitbourne, Stacey B., Brewer, Jessica V., Aslan, Mihaela, Connor, Todd, Argyres, Dean P., Stephens, Brady, Brophy, Mary T., Humphries, Donald E., Selva, Luis E., Do, Nhan, Shayan, Shahpoor, Cho, Kelly, Pyarajan, Saiju, Hauser, Elizabeth, Sun, Yan, Zhao, Hongyu, Wilson, Peter, McArdle, Rachel, Dellitalia, Louis, Mattocks, Kristin, Harley, John, Zablocki, Clement J., Whittle, Jeffrey, Jacono, Frank, Gutierrez, Salvador, Gibson, Gretchen, Hammer, Kimberly, Kaminsky, Laurence, Villareal, Gerardo, Kinlay, Scott, Xu, Junzhe, Hamner, Mark, Mathew, Roy, Bhushan, Sujata, Iruvanti, Pran, Godschalk, Michael, Ballas, Zuhair, Ivins, Douglas, Mastorides, Stephen, Moorman, Jonathan, Gappy, Saib, Klein, Jon, Ratcliffe, Nora, Florez, Hermes, Okusaga, Olaoluwa, Murdoch, Maureen, Sriram, Peruvemba, Yeh, Shing Shing, Tandon, Neeraj, Jhala, Darshana, Aguayo, Samuel, Cohen, David, Sharma, Satish, Liangpunsakul, Suthat, Oursler, Kris Ann, Whooley, Mary, Ahuja, Sunil, Constans, Joseph, Meyer, Paul, Greco, Jennifer, Rauchman, Michael, Servatius, Richard, Gaddy, Melinda, Wallbom, Agnes, Morgan, Timothy, Stapley, Todd, Sherman, Scott, Ross, George, Tsao, Philip, Strollo, Patrick, Boyko, Edward, Meyer, Laurence, Gupta, Samir, Huq, Mostaqul, Fayad, Joseph, Hung, Adriana, Lichy, Jack, Hurley, Robin, Robey, Brooks, Striker, Robert, Wray, Naomi R., Mattheisen, Manuel, Trzaskowski, Maciej, Byrne, Enda M., Abdellaoui, Abdel, Adams, Mark J., Agerbo, Esben, Air, Tracy M., Andlauer, Till F. M., Bacanu, Silviu-Alin, Bækvad-Hansen, Marie, Beekman, Aartjan T. F., Bigdeli, Tim B., Binder, Elisabeth B., Bryois, Julien, Buttenschøn, Henriette N., Bybjerg-Grauholm, Jonas, Cai, Na, Castelao, Enrique, Christensen, Jane Hvarregaard, Clarke, Toni-Kim, Coleman, Jonathan R. I., Colodro-Conde, Lucía, Couvy-Duchesne, Baptiste, Craddock, Nick, Crawford, Gregory E., Davies, Gail, Degenhardt, Franziska, Derks, Eske M., Direk, Nese, Dolan, Conor V., Dunn, Erin C., Eley, Thalia C., Escott-Price, Valentina, Hassan Kiadeh, Farnush Farhadi, Finucane, Hilary K., Foo, Jerome C., Forstner, Andreas J., Frank, Josef, Gaspar, Héléna A., Gill, Michael, Goes, Fernando S., Gordon, Scott D., Weinsheimer, Shantel Marie, Wellmann, Jürgen, Willemsen, Gonneke, Witt, Stephanie H., Wu, Yang, Xi, Hualin S., Yang, Jian, Zhang, Futao, Arolt, Volker, Baune, Bernhard T., Berger, Klaus, Boomsma, Dorret I., Cichon, Sven, Dannlowski, Udo, de Geus, E. J. C., DePaulo, J. Raymond, Domenici, Enrico, Domschke, Katharina, Esko, Tõnu, Grabe, Hans J., Hamilton, Steven P., Grove, Jakob, Hall, Lynsey S., Hansen, Christine Søholm, Hansen, Thomas F., Herms, Stefan, Hickie, Ian B., Hoffmann, Per, Homuth, Georg, Horn, Carsten, Hottenga, Jouke-Jan, Hougaard, David M., Howard, David M., Ising, Marcus, Jansen, Rick, Jones, Ian, Jones, Lisa A., Jorgenson, Eric, Knowles, James A., Kohane, Isaac S., Kraft, Julia, Kretzschmar, Warren W., Kutalik, Zoltán, Li, Yihan, Lind, Penelope A., MacIntyre, Donald J., MacKinnon, Dean F., Maier, Robert M., Maier, Wolfgang, Marchini, Jonathan, Mbarek, Hamdi, McGrath, Patrick, McGuffin, Peter, Medland, Sarah E., Mehta, Divya, Middeldorp, Christel M., Mihailov, Evelin, Milaneschi, Yuri, Milani, Lili, Mondimore, Francis M., Montgomery, Grant W., Mostafavi, Sara, Mullins, Niamh, Nauck, Matthias, Ng, Bernard, Nivard, Michel G., Nyholt, Dale R., O'Reilly, Paul F., Oskarsson, Hogni, Hayward, Caroline, Heath, Andrew C., Kendler, Kenneth S., Kloiber, Stefan, Lewis, Glyn, Li, Qingqin S., Lucae, Susanne, Madden, Pamela A. F., Magnusson, Patrik K., Martin, Nicholas G., McIntosh, Andrew M., Metspalu, Andres, Mors, Ole, Mortensen, Preben Bo, Müller-Myhsok, Bertram, Nordentoft, Merete, O'Donovan, Michael C., Paciga, Sara A., Pedersen, Nancy L., Owen, Michael J., Painter, Jodie N., Pedersen, Carsten Bøcker, Pedersen, Marianne Giørtz, Peterson, Roseann E., Peyrot, Wouter J., Pistis, Giorgio, Posthuma, Danielle, Quiroz, Jorge A., Qvist, Per, Rice, John P., Riley, Brien P., Rivera, Margarita, Mirza, Saira Saeed, Schoevers, Robert, Schulte, Eva C., Shen, Ling, Shi, Jianxin, Shyn, Stanley I., Sigurdsson, Engilbert, Sinnamon, Grant C. B., Smit, Johannes H., Smith, Daniel J., Stefansson, Hreinn, Steinberg, Stacy, Streit, Fabian, Strohmaier, Jana, Tansey, Katherine E., Teismann, Henning, Teumer, Alexander, Thompson, Wesley, Thomson, Pippa A., Thorgeirsson, Thorgeir E., Traylor, Matthew, Treutlein, Jens, Trubetskoy, Vassily, Uitterlinden, André G., Umbricht, Daniel, Van der Auwera, Sandra, van Hemert, Albert M., Viktorin, Alexander, Visscher, Peter M., Wang, Yunpeng, Webb, Bradley T., Penninx, Brenda W. J. H., Perlis, Roy H., Porteous, David J., Potash, James B., Preisig, Martin, Schaefer, Catherine, Schulze, Thomas G., Smoller, Jordan W., Stefansson, Kari, Tiemeier, Henning, Uher, Rudolf, Völzke, Henry, Weissman, Myrna M., Werge, Thomas, Lewis, Cathryn M., Levinson, Douglas F., Breen, Gerome, Børglum, Anders D., Sullivan, Patrick F., O'Connell, Kevin S., Coombes, Brandon, Qiao, Zhen, Als, Thomas D., Børte, Sigrid, Charney, Alexander W., Drange, Ole Kristian, Gandal, Michael J., Hagenaars, Saskia P., Ikeda, Masashi, Kamitaki, Nolan, Kim, Minsoo, Krebs, Kristi, Panagiotaropoulou, Georgia, Schilder, Brian M., Sloofman, Laura G., Winsvold, Bendik S., Won, Hong-Hee, Abramova, Liliya, Adorjan, Kristina, Al Eissa, Mariam, Albani, Diego, Alliey-Rodriguez, Ney, Anjorin, Adebayo, Antilla, Verneri, Antoniou, Anastasia, Awasthi, Swapnil, Baek, Ji Hyun, Bass, Nicholas, Bauer, Michael, Beins, Eva C., Bergen, Sarah E., Birner, Armin, Bøen, Erlend, Boks, Marco P., Bosch, Rosa, Brum, Murielle, Brumpton, Ben M., Brunkhorst-Kanaan, Nathalie, Budde, Monika, Byerley, William, Cairns, Murray, Casas, Miquel, Cervantes, Pablo, Cruceanu, Cristiana, Cuellar-Barboza, Alfredo, Cunningham, Julie, Curtis, David, Czerski, Piotr M., Dale, Anders M., Dalkner, Nina, David, Friederike S., Djurovic, Srdjan, Dobbyn, Amanda L., Douzenis, Athanassios, Elvsåshagen, Torbjørn, Ferrier, I. Nicol, Fiorentino, Alessia, Foroud, Tatiana M., Forty, Liz, Frei, Oleksandr, Freimer, Nelson B., Frisén, Louise, Gade, Katrin, Garnham, Julie, Gelernter, Joel, Gizer, Ian R., Gordon-Smith, Katherine, Greenwood, Tiffany A., Guzman-Parra, José, Ha, Kyooseob, Haraldsson, Magnus, Hautzinger, Martin, Heilbronner, Urs, Hellgren, Dennis, Holmans, Peter A., Huckins, Laura, Jamain, Stéphane, Johnson, Jessica S., Kalman, Janos L., Kamatani, Yoichiro, Kennedy, James L., Kittel-Schneider, Sarah, Kogevinas, Manolis, Koromina, Maria, Kranz, Thorsten M., Kranzler, Henry R., Kubo, Michiaki, Kupka, Ralph, Kushner, Steven A., Lavebratt, Catharina, Lawrence, Jacob, Leber, Markus, Lee, Heon-Jeong, Lee, Phil H., Levy, Shawn E., Lewis, Catrin, Liao, Calwing, Lundberg, Martin, Magnusson, Sigurdur H., Maihofer, Adam, Malaspina, Dolores, Maratou, Eirini, Martinsson, Lina, McGregor, Nathaniel W., McKay, James D., Medeiros, Helena, Millischer, Vincent, Moran, Jennifer L., Morris, Derek W., Mühleisen, Thomas W., O'Brien, Niamh, O'Donovan, Claire, Olde Loohuis, Loes M., Oruc, Lilijana, Papiol, Sergi, Pardiñas, Antonio F., Perry, Amy, Pfennig, Andrea, Porichi, Evgenia, Quested, Digby, Raj, Towfique, Rapaport, Mark H., Regeer, Eline J., Rivas, Fabio, Roth, Julian, Roussos, Panos, Ruderfer, Douglas M., Sánchez-Mora, Cristina, Senner, Fanny, Sharp, Sally, Shilling, Paul D., Sirignano, Lea, Slaney, Claire, Smeland, Olav B., Sobell, Janet L., Artigas, Maria Soler, Spijker, Anne T., Stein, Dan J., Strauss, John S., Świątkowska, Beata, Terao, Chikashi, Toma, Claudio, Tooney, Paul, Tsermpini, Evangelia-Eirini, Vawter, Marquis P., Vedder, Helmut, Walters, James T. R., Xi, Simon, Xu, Wei, Kay Yang, Jessica Mei, Young, Allan H., Young, Hannah, Zandi, Peter P., Zhou, Hang, Zillich, Lea, Adolfsson, Rolf, Agartz, Ingrid, Alda, Martin, Alfredsson, Lars, Babadjanova, Gulja, Backlund, Lena, Bellivier, Frank, Bengesser, Susanne, Berrettini, Wade H., Blackwood, Douglas H. R., Boehnke, Michael, Carr, Vaughan J., Catts, Stanley, Corvin, Aiden, Craddock, Nicholas, Dikeos, Dimitris, Etain, Bruno, Ferentinos, Panagiotis, Frye, Mark, Fullerton, Janice M., Gawlik, Micha, Gershon, Elliot S., Green, Melissa J., Grigoroiu-Serbanescu, Maria, Hauser, Joanna, Henskens, Frans, Hillert, Jan, Hong, Kyung Sue, Hultman, Christina M., Hveem, Kristian, Iwata, Nakao, Jablensky, Assen V., Kahn, René S., Kelsoe, John R., Kirov, George, Landén, Mikael, Leboyer, Marion, Lissowska, Jolanta, Lochner, Christine, Loughland, Carmel, Mathews, Carol A., Mayoral, Fermin, McElroy, Susan L., McMahon, Francis J., Melle, Ingrid, Michie, Patricia, Mitchell, Philip B., Morken, Gunnar, Mowry, Bryan, Myers, Richard M., Neale, Benjamin M., Nievergelt, Caroline M., Oedegaard, Ketil J., Olsson, Tomas, Pantelis, Chris, Pato, Carlos, Pato, Michele T., Patrinos, George P., Ramos-Quiroga, Josep Antoni, Reif, Andreas, Reininghaus, Eva Z., Ribasés, Marta, Rouleau, Guy A., Saito, Takeo, Schall, Ulrich, Schalling, Martin, Schofield, Peter R., Scott, Laura J., Scott, Rodney J., Serretti, Alessandro, Weickert, Cynthia Shannon, Stordal, Eystein, Turecki, Gustavo, Vaaler, Arne E., Vieta, Eduard, Vincent, John B., Waldman, Irwin D., Weickert, Thomas W., Zwart, John-Anker, Biernacka, Joanna M., Nurnberger, John I., Edenberg, Howard J., Stahl, Eli A., McQuillin, Andrew, Di Florio, Arianna, Ophoff, Roel A., Andreassen, Ole A., Adan, Roger A. H., Ando, Tetsuya, Aschauer, Harald, Baker, Jessica H., Bencko, Vladimir, Bergen, Andrew W., Birgegård, Andreas, Boden, Joseph M., Boehm, Ilka, Boni, Claudette, Perica, Vesna Boraska, Brandt, Harry, Buehren, Katharina, Bulik, Cynthia M., Burghardt, Roland, Carlberg, Laura, Cassina, Matteo, Clementi, Maurizio, Cone, Roger D., Courtet, Philippe, Crawford, Steven, Crow, Scott, Crowley, James J., Danner, Unna N., Davis, Oliver S. P., de Zwaan, Martina, Dedoussis, George, Degortes, Daniela, DeSocio, Janiece E., Dick, Danielle M., Dina, Christian, Dmitrzak-Weglarz, Monika, Martinez, Elisa Docampo, Duncan, Laramie E., Egberts, Karin, Marshall, Christian R., Mattingsdal, Morten, McDevitt, Sara, Meulenbelt, Ingrid, Micali, Nadia, Mitchell, James, Mitchell, Karen, Monteleone, Palmiero, Monteleone, Alessio Maria, Munn-Chernoff, Melissa A., Nacmias, Benedetta, Navratilova, Marie, Ntalla, Ioanna, Olsen, Catherine M., O'Toole, Julie K., Padyukov, Leonid, Palotie, Aarno, Pantel, Jacques, Papezova, Hana, Parker, Richard, Pearson, John F., Ehrlich, Stefan, Escaramís, Geòrgia, Espeseth, Thomas, Estivill, Xavier, Farmer, Anne, Favaro, Angela, Fernández-Aranda, Fernando, Fichter, Manfred M., Fischer, Krista, Floyd, James A. B., Föcker, Manuel, Foretova, Lenka, Forzan, Monica, Franklin, Christopher S., Gallinger, Steven, Gambaro, Giovanni, Giegling, Ina, Giuranna, Johanna, Giusti-Rodríquez, Paola, Gonidakis, Fragiskos, Gordon, Scott, Gorwood, Philip, Mayora, Monica Gratacos, Guillaume, Sébastien, Guo, Yiran, Hakonarson, Hakon, Halmi, Katherine A., Hanscombe, Ken B., Hatzikotoulas, Konstantinos, Hebebrand, Johannes, Helder, Sietske G., Henders, Anjali K., Herpertz-Dahlmann, Beate, Herzog, Wolfgang, Hinney, Anke, Horwood, L. John, Hübel, Christopher, Petersen, Liselotte V., Pinto, Dalila, Purves, Kirstin L., Raevuori, Anu, Ramoz, Nicolas, Reichborn-Kjennerud, Ted, Ricca, Valdo, Ripatti, Samuli, Ritschel, Franziska, Roberts, Marion, Rybakowski, Filip, Santonastaso, Paolo, Scherag, André, Scherer, Stephen W., Schmidt, Ulrike, Schork, Nicholas J., Schosser, Alexandra, Seitz, Jochen, Slachtova, Lenka, Slagboom, P. Eline, Slof-Op 't Landt, Margarita C. T., Slopien, Agnieszka, Soranzo, Nicole, Sorbi, Sandro, Southam, Lorraine, Steen, Vidar W., Strober, Michael, Huckins, Laura M., Hudson, James I., Imgart, Hartmut, Inoko, Hidetoshi, Janout, Vladimir, Jiménez-Murcia, Susana, Johnson, Craig, Jordan, Jennifer, Julià, Antonio, Kalsi, Gursharan, Kaminská, Deborah, Kaplan, Allan S., Kaprio, Jaakko, Karhunen, Leila, Karwautz, Andreas, Kas, Martien J. H., Kaye, Walter H., Kennedy, Martin A., Keski-Rahkonen, Anna, Kiezebrink, Kirsty, Kim, Youl-Ri, Kirk, Katherine M., Klareskog, Lars, Klump, Kelly L., Knudsen, Gun Peggy S., Larsen, Janne T., Le Hellard, Stephanie, Leppä, Virpi M., Li, Dong, Lichtenstein, Paul, Lilenfeld, Lisa, Lin, Bochao Danae, Lundervold, Astri, Luykx, Jurjen, Magistretti, Pierre J., Maj, Mario, Mannik, Katrin, Marsal, Sara, Stuber, Garret D., Szatkiewicz, Jin P., Tachmazidou, Ioanna, Tenconi, Elena, Thornton, Laura M., Tortorella, Alfonso, Tozzi, Federica, Treasure, Janet, Tsitsika, Artemis, Tyszkiewicz-Nwafor, Marta, Tziouvas, Konstantinos, van Elburg, Annemarie A., van Furth, Eric F., Wade, Tracey D., Wagner, Gudrun, Walton, Esther, Watson, Hunna J., Whiteman, David C., Wichmann, H. Erich, Widen, Elisabeth, Woodside, D. Blake, Yao, Shuyang, Yilmaz, Zeynep, Zeggini, Eleftheria, Zerwas, Stephanie, Zipfel, Stephan, Jungkunz, Martin, Mullins, N., Kang, J., Campos, A. I., Coleman, J. R. I., Edwards, A. C., Galfalvy, H., Levey, D. F., Lori, A., Shabalin, A., Starnawska, A., Su, M. -H., Watson, H. J., Adams, M., Awasthi, S., Gandal, M., Hafferty, J. D., Hishimoto, A., Kim, M., Okazaki, S., Otsuka, I., Ripke, S., Ware, E. B., Bergen, A. W., Berrettini, W. H., Bohus, M., Brandt, H., Chang, X., Chen, W. J., Chen, H. -C., Crawford, S., Crow, S., Diblasi, E., Duriez, P., Fernandez-Aranda, F., Fichter, M. M., Gallinger, S., Glatt, S. J., Gorwood, P., Guo, Y., Hakonarson, H., Halmi, K. A., Hwu, H. -G., Jain, S., Jamain, S., Jimenez-Murcia, S., Johnson, C., Kaplan, A. S., Kaye, W. H., Keel, P. K., Kennedy, J. L., Klump, K. L., Li, D., Liao, S. -C., Lieb, K., Lilenfeld, L., Liu, C. -M., Magistretti, P. J., Marshall, C. R., Mitchell, J. E., Monson, E. T., Myers, R. M., Pinto, D., Powers, A., Ramoz, N., Roepke, S., Rozanov, V., Scherer, S. W., Schmahl, C., Sokolowski, M., Strober, M., Thornton, L. M., Treasure, J., Tsuang, M. T., Witt, S. H., Woodside, D. B., Yilmaz, Z., Zillich, L., Adolfsson, R., Agartz, I., Air, T. M., Alda, M., Alfredsson, L., Andreassen, O. A., Anjorin, A., Appadurai, V., Soler Artigas, M., Van der Auwera, S., Azevedo, M. H., Bass, N., Bau, C. H. D., Baune, B. T., Bellivier, F., Berger, K., Biernacka, J. M., Bigdeli, T. B., Binder, E. B., Boehnke, M., Boks, M. P., Bosch, R., Braff, D. L., Bryant, R., Budde, M., Byrne, E. M., Cahn, W., Casas, M., Castelao, E., Cervilla, J. A., Chaumette, B., Cichon, S., Corvin, A., Craddock, N., Craig, D., Degenhardt, F., Djurovic, S., Edenberg, H. J., Fanous, A. H., Foo, J. C., Forstner, A. J., Frye, M., Fullerton, J. M., Gatt, J. M., Gejman, P. V., Giegling, I., Grabe, H. J., Green, M. J., Grevet, E. H., Grigoroiu-Serbanescu, M., Gutierrez, B., Guzman-Parra, J., Hamilton, S. P., Hamshere, M. L., Hartmann, A., Hauser, J., Heilmann-Heimbach, S., Hoffmann, P., Ising, M., Jones, I., Jones, L. A., Jonsson, L., Kahn, R. S., Kelsoe, J. R., Kendler, K. S., Kloiber, S., Koenen, K. C., Kogevinas, M., Konte, B., Krebs, M. -O., Landen, M., Lawrence, J., Leboyer, M., Lee, P. H., Levinson, D. F., Liao, C., Lissowska, J., Lucae, S., Mayoral, F., Mcelroy, S. L., Mcgrath, P., Mcguffin, P., Mcquillin, A., Medland, S. E., Mehta, D., Melle, I., Milaneschi, Y., Mitchell, P. B., Molina, E., Morken, G., Mortensen, P. B., Muller-Myhsok, B., Nievergelt, C., Nimgaonkar, V., Nothen, M. M., O'Donovan, M. C., Ophoff, R. A., Owen, M. J., Pato, C., Pato, M. T., Penninx, B. W. J. H., Pimm, J., Pistis, G., Potash, J. B., Power, R. A., Preisig, M., Quested, D., Ramos-Quiroga, J. A., Reif, A., Ribases, M., Richarte, V., Rietschel, M., Rivera, M., Roberts, A., Roberts, G., Rouleau, G. A., Rovaris, D. L., Rujescu, D., Sanchez-Mora, C., Sanders, A. R., Schofield, P. R., Schulze, T. G., Scott, L. J., Serretti, A., Shi, J., Shyn, S. I., Sirignano, L., Sklar, P., Smeland, O. B., Smoller, J. W., Sonuga-Barke, E. J. S., Spalletta, G., Strauss, J. S., Swiatkowska, B., Trzaskowski, M., Turecki, G., Vilar-Ribo, L., Vincent, J. B., Volzke, H., Walters, J. T. R., Shannon Weickert, C., Weickert, T. W., Weissman, M. M., Williams, L. M., Wray, N. R., Zai, C. C., Ashley-Koch, A. E., Beckham, J. C., Hauser, E. R., Hauser, M. A., Kimbrel, N. A., Lindquist, J. H., Mcmahon, B., Oslin, D. W., Qin, X., Mattheisen, M., Abdellaoui, A., Adams, M. J., Agerbo, E., Andlauer, T. F. M., Bacanu, S. -A., Baekvad-Hansen, M., Beekman, A. T. F., Bryois, J., Buttenschon, H. N., Bybjerg-Grauholm, J., Cai, N., Christensen, J. H., Clarke, T. -K., Colodro-Conde, L., Couvy-Duchesne, B., Crawford, G. E., Davies, G., Derks, E. M., Direk, N., Dolan, C. V., Dunn, E. C., Eley, T. C., Escott-Price, V., Hassan Kiadeh, F. F., Finucane, H. K., Frank, J., Gaspar, H. A., Gill, M., Goes, F. S., Gordon, S. D., Weinsheimer, S. M., Wellmann, J., Willemsen, G., Wu, Y., Xi, H. S., Yang, J., Zhang, F., Arolt, V., Boomsma, D. I., Dannlowski, U., Depaulo, J. R., Domenici, E., Domschke, K., Esko, T., Grove, J., Hall, L. S., Hansen, C. S., Hansen, T. F., Herms, S., Hickie, I. B., Homuth, G., Horn, C., Hottenga, J. -J., Hougaard, D. M., Howard, D. M., Jansen, R., Jorgenson, E., Knowles, J. A., Kohane, I. S., Kraft, J., Kretzschmar, W. W., Kutalik, Z., Li, Y., Lind, P. A., Macintyre, D. J., Mackinnon, D. F., Maier, R. M., Maier, W., Marchini, J., Mbarek, H., Middeldorp, C. M., Mihailov, E., Milani, L., Mondimore, F. M., Montgomery, G. W., Mostafavi, S., Nauck, M., Ng, B., Nivard, M. G., Nyholt, D. R., O'Reilly, P. F., Oskarsson, H., Hayward, C., Heath, A. C., Lewis, G., Li, Q. S., Madden, P. A. F., Magnusson, P. K., Martin, N. G., Mcintosh, A. M., Metspalu, A., Mors, O., Nordentoft, M., Paciga, S. A., Pedersen, N. L., Painter, J. N., Pedersen, C. B., Pedersen, M. G., Peterson, R. E., Peyrot, W. J., Posthuma, D., Quiroz, J. A., Qvist, P., Rice, J. P., Riley, B. P., Mirza, S. S., Schoevers, R., Schulte, E. C., Shen, L., Sigurdsson, E., Sinnamon, G. C. B., Smit, J. H., Smith, D. J., Stefansson, H., Steinberg, S., Streit, F., Strohmaier, J., Tansey, K. E., Teismann, H., Teumer, A., Thompson, W., Thomson, P. A., Thorgeirsson, T. E., Traylor, M., Treutlein, J., Trubetskoy, V., Uitterlinden, A. G., Umbricht, D., der Auwera, S. V., van Hemert, A. M., Viktorin, A., Visscher, P. M., Wang, Y., Webb, B. T., Perlis, R. H., Porteous, D. J., Schaefer, C., Stefansson, K., Tiemeier, H., Uher, R., Werge, T., Lewis, C. M., Breen, G., Borglum, A. D., Sullivan, P. F., O'Connell, K. S., Coombes, B., Qiao, Z., Als, T. D., Borte, S., Charney, A. W., Drange, O. K., Gandal, M. J., Hagenaars, S. P., Ikeda, M., Kamitaki, N., Krebs, K., Panagiotaropoulou, G., Schilder, B. M., Sloofman, L. G., Winsvold, B. S., Won, H. -H., Abramova, L., Adorjan, K., Al Eissa, M., Albani, D., Alliey-Rodriguez, N., Antilla, V., Antoniou, A., Baek, J. H., Bauer, M., Beins, E. C., Bergen, S. E., Birner, A., Boen, E., Brum, M., Brumpton, B. M., Brunkhorst-Kanaan, N., Byerley, W., Cairns, M., Cervantes, P., Cruceanu, C., Cuellar-Barboza, A., Cunningham, J., Curtis, D., Czerski, P. M., Dale, A. M., Dalkner, N., David, F. S., Dobbyn, A. L., Douzenis, A., Elvsashagen, T., Ferrier, I. N., Fiorentino, A., Foroud, T. M., Forty, L., Frei, O., Freimer, N. B., Frisen, L., Gade, K., Garnham, J., Gelernter, J., Gizer, I. R., Gordon-Smith, K., Greenwood, T. A., Ha, K., Haraldsson, M., Hautzinger, M., Heilbronner, U., Hellgren, D., Holmans, P. A., Huckins, L., Johnson, J. S., Kalman, J. L., Kamatani, Y., Kittel-Schneider, S., Koromina, M., Kranz, T. M., Kranzler, H. R., Kubo, M., Kupka, R., Kushner, S. A., Lavebratt, C., Leber, M., Lee, H. -J., Levy, S. E., Lewis, C., Lundberg, M., Magnusson, S. H., Maihofer, A., Malaspina, D., Maratou, E., Martinsson, L., Mcgregor, N. W., Mckay, J. D., Medeiros, H., Millischer, V., Moran, J. L., Morris, D. W., Muhleisen, T. 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Z., Saito, T., Schall, U., Schalling, M., Scott, R. J., Weickert, C. S., Stordal, E., Vaaler, A. E., Vieta, E., Waldman, I. D., Zwart, J. -A., Nurnberger, J. I., Stahl, E. A., Di Florio, A., Adan, R. A. H., Ando, T., Aschauer, H., Baker, J. H., Bencko, V., Birgegard, A., Boden, J. M., Boehm, I., Boni, C., Perica, V. B., Buehren, K., Bulik, C. M., Burghardt, R., Carlberg, L., Cassina, M., Clementi, M., Cone, R. D., Courtet, P., Crowley, J. J., Danner, U. N., Davis, O. S. P., de Zwaan, M., Dedoussis, G., Degortes, D., Desocio, J. E., Dick, D. M., Dina, C., Dmitrzak-Weglarz, M., Martinez, E. D., Duncan, L. E., Egberts, K., Mattingsdal, M., Mcdevitt, S., Meulenbelt, I., Micali, N., Mitchell, J., Mitchell, K., Monteleone, P., Monteleone, A. M., Munn-Chernoff, M. A., Nacmias, B., Navratilova, M., Ntalla, I., Olsen, C. M., O'Toole, J. K., Padyukov, L., Palotie, A., Pantel, J., Papezova, H., Parker, R., Pearson, J. 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P., Stephens, B., Brophy, M. T., Humphries, D. E., Selva, L. E., Do, N., Shayan, S., Cho, K., Pyarajan, S., Hauser, E., Sun, Y., Zhao, H., Wilson, P., Mcardle, R., Dellitalia, L., Mattocks, K., Harley, J., Zablocki, C. J., Whittle, J., Jacono, F., Gutierrez, S., Gibson, G., Hammer, K., Kaminsky, L., Villareal, G., Kinlay, S., Xu, J., Hamner, M., Mathew, R., Bhushan, S., Iruvanti, P., Godschalk, M., Ballas, Z., Ivins, D., Mastorides, S., Moorman, J., Gappy, S., Klein, J., Ratcliffe, N., Florez, H., Okusaga, O., Murdoch, M., Sriram, P., Yeh, S. S., Tandon, N., Jhala, D., Aguayo, S., Cohen, D., Sharma, S., Liangpunsakul, S., Oursler, K. A., Whooley, M., Ahuja, S., Constans, J., Meyer, P., Greco, J., Rauchman, M., Servatius, R., Gaddy, M., Wallbom, A., Morgan, T., Stapley, T., Sherman, S., Ross, G., Tsao, P., Strollo, P., Boyko, E., Meyer, L., Gupta, S., Huq, M., Fayad, J., Hung, A., Lichy, J., Hurley, R., Robey, B., Striker, R., Erlangsen, A., Kessler, R. C., Porteous, D., Ursano, R. J., Wasserman, D., Coon, H., Demontis, D., Docherty, A. R., Kuo, P. -H., Mann, J. J., Renteria, M. E., Stein, M. B., Willour, V., Psychiatry, Biological Psychology, APH - Methodology, APH - Mental Health, APH - Health Behaviors & Chronic Diseases, AMS - Sports, AMS - Ageing & Vitality, APH - Personalized Medicine, Amsterdam Neuroscience - Complex Trait Genetics, Complex Trait Genetics, Institute for Molecular Medicine Finland, Centre of Excellence in Complex Disease Genetics, Aarno Palotie / Principal Investigator, Genomics of Neurological and Neuropsychiatric Disorders, HUS Psychiatry, Department of Public Health, Clinicum, Nuorisopsykiatria, Faculty Common Matters (Faculty of Social Sciences), Samuli Olli Ripatti / Principal Investigator, Complex Disease Genetics, Biostatistics Helsinki, Anna Keski-Rahkonen / Principal Investigator, Elisabeth Ingrid Maria Widen / Principal Investigator, Genomic Discoveries and Clinical Translation, Internal medicine, Amsterdam Neuroscience - Mood, Anxiety, Psychosis, Stress & Sleep, APH - Digital Health, Mullins N., Kang J., Campos A.I., Coleman J.R.I., Edwards A.C., Galfalvy H., Levey D.F., Lori A., Shabalin A., Starnawska A., Su M.-H., Watson H.J., Adams M., Awasthi S., Gandal M., Hafferty J.D., Hishimoto A., Kim M., Okazaki S., Otsuka I., Ripke S., Ware E.B., Bergen A.W., Berrettini W.H., Bohus M., Brandt H., Chang X., Chen W.J., Chen H.-C., Crawford S., Crow S., DiBlasi E., Duriez P., Fernandez-Aranda F., Fichter M.M., Gallinger S., Glatt S.J., Gorwood P., Guo Y., Hakonarson H., Halmi K.A., Hwu H.-G., Jain S., Jamain S., Jimenez-Murcia S., Johnson C., Kaplan A.S., Kaye W.H., Keel P.K., Kennedy J.L., Klump K.L., Li D., Liao S.-C., Lieb K., Lilenfeld L., Liu C.-M., Magistretti P.J., Marshall C.R., Mitchell J.E., Monson E.T., Myers R.M., Pinto D., Powers A., Ramoz N., Roepke S., Rozanov V., Scherer S.W., Schmahl C., Sokolowski M., Strober M., Thornton L.M., Treasure J., Tsuang M.T., Witt S.H., Woodside D.B., Yilmaz Z., Zillich L., Adolfsson R., Agartz I., Air T.M., Alda M., Alfredsson L., Andreassen O.A., Anjorin A., Appadurai V., Soler Artigas M., Van der Auwera S., Azevedo M.H., Bass N., Bau C.H.D., Baune B.T., Bellivier F., Berger K., Biernacka J.M., Bigdeli T.B., Binder E.B., Boehnke M., Boks M.P., Bosch R., Braff D.L., Bryant R., Budde M., Byrne E.M., Cahn W., Casas M., Castelao E., Cervilla J.A., Chaumette B., Cichon S., Corvin A., Craddock N., Craig D., Degenhardt F., Djurovic S., Edenberg H.J., Fanous A.H., Foo J.C., Forstner A.J., Frye M., Fullerton J.M., Gatt J.M., Gejman P.V., Giegling I., Grabe H.J., Green M.J., Grevet E.H., Grigoroiu-Serbanescu M., Gutierrez B., Guzman-Parra J., Hamilton S.P., Hamshere M.L., Hartmann A., Hauser J., Heilmann-Heimbach S., Hoffmann P., Ising M., Jones I., Jones L.A., Jonsson L., Kahn R.S., Kelsoe J.R., Kendler K.S., Kloiber S., Koenen K.C., Kogevinas M., Konte B., Krebs M.-O., Landen M., Lawrence J., Leboyer M., Lee P.H., Levinson D.F., Liao C., Lissowska J., Lucae S., Mayoral F., McElroy S.L., McGrath P., McGuffin P., McQuillin A., Medland S.E., Mehta D., Melle I., 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Maratou E., Martinsson L., McGregor N.W., McKay J.D., Medeiros H., Millischer V., Moran J.L., Morris D.W., Muhleisen T.W., O'Brien N., O'Donovan C., Olde Loohuis L.M., Oruc L., Papiol S., Pardinas A.F., Perry A., Pfennig A., Porichi E., Raj T., Rapaport M.H., Regeer E.J., Rivas F., Roth J., Roussos P., Ruderfer D.M., Senner F., Sharp S., Shilling P.D., Slaney C., Sobell J.L., Artigas M.S., Spijker A.T., Stein D.J., Terao C., Toma C., Tooney P., Tsermpini E.-E., Vawter M.P., Vedder H., Xi S., Xu W., Kay Yang J.M., Young A.H., Young H., Zandi P.P., Zhou H., HUNT All-In Psychiatry, Babadjanova G., Backlund L., Bengesser S., Blackwood D.H.R., Carr V.J., Catts S., Dikeos D., Etain B., Ferentinos P., Gawlik M., Gershon E.S., Henskens F., Hillert J., Hong K.S., Hultman C.M., Hveem K., Iwata N., Jablensky A.V., Kirov G., Lochner C., Loughland C., Mathews C.A., McMahon F.J., Michie P., Mowry B., Neale B.M., Nievergelt C.M., Oedegaard K.J., Olsson T., Pantelis C., Patrinos G.P., Reininghaus E.Z., Saito T., Schall U., Schalling M., Scott R.J., Weickert C.S., Stordal E., Vaaler A.E., Vieta E., Waldman I.D., Zwart J.-A., Nurnberger J.I., Stahl E.A., Di Florio A., Adan R.A.H., Ando T., Aschauer H., Baker J.H., Bencko V., Birgegard A., Boden J.M., Boehm I., Boni C., Perica V.B., Buehren K., Bulik C.M., Burghardt R., Carlberg L., Cassina M., Clementi M., Cone R.D., Courtet P., Crowley J.J., Danner U.N., Davis O.S.P., de Zwaan M., Dedoussis G., Degortes D., DeSocio J.E., Dick D.M., Dina C., Dmitrzak-Weglarz M., Martinez E.D., Duncan L.E., Egberts K., Mattingsdal M., McDevitt S., Meulenbelt I., Micali N., Mitchell J., Mitchell K., Monteleone P., Monteleone A.M., Munn-Chernoff M.A., Nacmias B., Navratilova M., Ntalla I., Olsen C.M., O'Toole J.K., Padyukov L., Palotie A., Pantel J., Papezova H., Parker R., Pearson J.F., Ehrlich S., Escaramis G., Espeseth T., Estivill X., Farmer A., Favaro A., Fischer K., Floyd J.A.B., Focker M., Foretova L., Forzan M., Franklin C.S., Gambaro G., Giuranna J., Giusti-Rodriquez P., Gonidakis F., Gordon S., Mayora M.G., Guillaume S., Hanscombe K.B., Hatzikotoulas K., Hebebrand J., Helder S.G., Henders A.K., Herpertz-Dahlmann B., Herzog W., Hinney A., Horwood L.J., Hubel C., Petersen L.V., Purves K.L., Raevuori A., Reichborn-Kjennerud T., Ricca V., Ripatti S., Ritschel F., Roberts M., Rybakowski F., Santonastaso P., Scherag A., Schmidt U., Schork N.J., Schosser A., Seitz J., Slachtova L., Slagboom P.E., Slof-Op 't Landt M.C.T., Slopien A., Soranzo N., Sorbi S., Southam L., Steen V.W., Huckins L.M., Hudson J.I., Imgart H., Inoko H., Janout V., Jordan J., Julia A., Kalsi G., Kaminska D., Kaprio J., Karhunen L., Karwautz A., Kas M.J.H., Kennedy M.A., Keski-Rahkonen A., Kiezebrink K., Kim Y.-R., Kirk K.M., Klareskog L., Knudsen G.P.S., Larsen J.T., Le Hellard S., Leppa V.M., Lichtenstein P., Lin B.D., Lundervold A., Luykx J., Maj M., Mannik K., Marsal S., Stuber G.D., Szatkiewicz J.P., Tachmazidou I., Tenconi E., Tortorella A., Tozzi F., Tsitsika A., Tyszkiewicz-Nwafor M., Tziouvas K., van Elburg A.A., van Furth E.F., Wade T.D., Wagner G., Walton E., Whiteman D.C., Wichmann H.E., Widen E., Yao S., Zeggini E., Zerwas S., Zipfel S., Jungkunz M., Dietl L., Schwarze C.E., Dahmen N., Schott B.H., Mobascher A., Crivelli S., Dennis M.F., Harvey P.D., Carter B.W., Huffman J.E., Jacobson D., Madduri R., Olsen M.K., Pestian J., Gaziano J.M., Muralidhar S., Ramoni R., Beckham J., Chang K.-M., O'Donnell C.J., Tsao P.S., Breeling J., Huang G., Romero J.P.C., Moser J., Whitbourne S.B., Brewer J.V., Aslan M., Connor T., Argyres D.P., Stephens B., Brophy M.T., Humphries D.E., Selva L.E., Do N., Shayan S., Cho K., Pyarajan S., Hauser E., Sun Y., Zhao H., Wilson P., McArdle R., Dellitalia L., Mattocks K., Harley J., Zablocki C.J., Whittle J., Jacono F., Gutierrez S., Gibson G., Hammer K., Kaminsky L., Villareal G., Kinlay S., Xu J., Hamner M., Mathew R., Bhushan S., Iruvanti P., Godschalk M., Ballas Z., Ivins D., Mastorides S., Moorman J., Gappy S., Klein J., Ratcliffe N., Florez H., Okusaga O., Murdoch M., Sriram P., Yeh S.S., Tandon N., Jhala D., Aguayo S., Cohen D., Sharma S., Liangpunsakul S., Oursler K.A., Whooley M., Ahuja S., Constans J., Meyer P., Greco J., Rauchman M., Servatius R., Gaddy M., Wallbom A., Morgan T., Stapley T., Sherman S., Ross G., Tsao P., Strollo P., Boyko E., Meyer L., Gupta S., Huq M., Fayad J., Hung A., Lichy J., Hurley R., Robey B., Striker R., Erlangsen A., Kessler R.C., Porteous D., Ursano R.J., Wasserman D., Coon H., Demontis D., Docherty A.R., Kuo P.-H., Mann J.J., Renteria M.E., Stein M.B., and Willour V.
Subjects: LD SCORE REGRESSION, Genome-wide association study, Suicide, Attempted, 3124 Neurology and psychiatry, 0302 clinical medicine, Risk Factors, Insomnia, Suicide attempt, GWAS, Suïcidi, Depression (differential diagnoses), Cause of death, Psychiatry, 0303 health sciences, Factors de risc en les malalties, Mental Disorders, Genetic Correlation, Genome-wide Association Study, Pleiotropy, Polygenicity, Suicide, Suicide Attempt, DEPRESSION, 3. Good health, Genetic correlation, Genome-Wide Association Study, Humans, Polymorphism, Single Nucleotide, Depressive Disorder, Major, Mental illness, Cohort, SEX, medicine.symptom, Human, medicine.medical_specialty, Risk factors in diseases, BF, Locus (genetics), BEHAVIORS, Psykiatri, EVENTS, 03 medical and health sciences, SDG 3 - Good Health and Well-being, medicine, ddc:610, GENOME-WIDE ASSOCIATION, IDEATION, Socioeconomic status, METAANALYSIS, Biological Psychiatry, 030304 developmental biology, business.industry, Risk Factor, Genetic architecture, THOUGHTS, RC0321, business, Malalties mentals, 030217 neurology & neurosurgery
Abstract: Statistical analyses were carried out on the NL Genetic Cluster Computer (http://www.geneticcluster.org) hosted by SURFsara and the Mount Sinai high performance computing cluster (http://hpc.mssm.edu), which is supported by the Office of Research Infrastructure of the National Institutes of Health (Grant Nos. S10OD018522 and S10OD026880). This work was conducted in part using the resources of the Advanced Computing Center for Research and Education at Vanderbilt University, Nashville, TN. This work was funded by the National Institutes of Health (Grant Nos. R01MH116269 and R01MH121455 [to DMR]), NIGMS of the National Institutes of Health (Grant No. T32GM007347 [to JK]), and the Brain & Behavior Research Foundation (NARSAD Young Investigator Award No. 29551 [to NM])., BACKGROUND: Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. METHODS: We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. RESULTS: Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. CONCLUSIONS: Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders., Office of Research Infrastructure of the National Institutes of Health S10OD018522 S10OD026880, United States Department of Health & Human Services, National Institutes of Health (NIH) - USA R01MH116269 R01MH121455, NIH National Institute of General Medical Sciences (NIGMS) T32GM007347 NARSAD 29551
Published: 2022
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11. Analysis of structural brain asymmetries in attention-deficit/hyperactivity disorder in 39 datasets

Author: Dirk J. Heslenfeld, Merel Postema, Paul M. Thompson, Sarah Baumeister, Tiffany M. Chaim-Avancini, Catharina A. Hartman, Sara Lera-Miguel, Patrick de Zeeuw, Sara Ambrosino, Neil A. Harrison, Marcus V. Zanetti, Philip Asherson, Joel T. Nigg, Liesbeth Reneman, David Coghill, Gustavo Sudre, Alysa E. Doyle, Francisco X. Castellanos, Tobias Banaschewski, Oscar Vilarroya, Mario Rodrigues Louzã, Kaylita Chantiluke, Annette Conzelmann, Georg G. von Polier, Lizanne J. S. Schweren, Anastasia Christakou, Klaus-Peter Lesch, Sarah Durston, Simon E. Fisher, Yuliya N. Yoncheva, Jochen Seitz, David C. Glahn, Timothy J. Silk, Norbert Skokauskas, Mark A. Bellgrove, Damien A. Fair, Geraldo F. Busatto, Georg C. Ziegler, Eric Earl, Yannis Paloyelis, Jeffery N. Epstein, Jaap Oosterlaan, Clare Kelly, Paulo Mattos, Gregor Kohls, Jan Haavik, Joseph Biederman, Janita Bralten, Neda Jahanshad, Claiton H.D. Bau, Thomas Ethofer, Paul Pauli, Cibele Edom Bandeira, Andreas Reif, Pieter J. Hoekstra, Theo G.M. van Erp, Susanne Walitza, Marie F. Høvik, Sarah Hohmann, Barbara Franke, Luisa Lázaro, Thomas Frodl, Tinatin Gogberashvili, Jonna Kuntsi, J. Antoni Ramos-Quiroga, Daniel Brandeis, Stephanie E. Novotny, Martine Hoogman, Juan Carlos Soliva Vila, Anouk Schrantee, Rosa Nicolau, Kerstin Konrad, Eileen Oberwelland Weiss, Ruth O'Gorman Tuura, Bernd Kardatzki, Felipe Almeida Picon, Hazel McCarthy, Yolanda Vives-Gilabert, Ana Cubillo, Charles B Malpas, Mara Cercignani, Astri J. Lundervold, Michael C. Stevens, Eugenio H. Grevet, Katya Rubia, Renata B. Cupertino, Philip Shaw, Georgii Karkashadze, Fernanda Tovar-Moll, Bob Oranje, Leyla Namazova-Baranova, A.A. Baranov, Andreas J. Fallgatter, Leanne Tamm, Terry L. Jernigan, Matt C. Gabel, Clyde Francks, Pedro G.P. Rosa, Stephen V. Faraone, Jan K. Buitelaar, Kerstin J. Plessen, Silvia Brem, Sarah E. Medland, Alasdair Vance, Ramona Baur-Streubel, ENIGMA ADHD Working Group, General Paediatrics, ARD - Amsterdam Reproduction and Development, Radiology and Nuclear Medicine, APH - Mental Health, APH - Personalized Medicine, ANS - Brain Imaging, ANS - Compulsivity, Impulsivity & Attention, Institut Català de la Salut, [Postema MC] Language and Genetics Department, Max Planck Institute for Psycholinguistics, Nijmegen, The Netherlands. [Hoogman M] Department of Human Genetics, Radboud University Medical Center, Nijmegen, Netherlands. Donders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, Netherlands. [Ambrosino S] NICHE lab, Department of Psychiatry, University Medical Center Utrecht Brain Center, Utrecht University, Utrecht, The Netherlands. [Asherson P] Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, UK. [Banaschewski T] Department of Child and Adolescent Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim/Heidelberg University, Mannheim, Germany. [Bandeira CE] Adulthood ADHD Outpatient Program (ProDAH), Clinical Research Center, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil. Department of Genetics, Institute of Biosciences, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil. [Ramos-Quiroga JA] Servei de Psiquiatria, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Grup de Recerca en Psiquiatria, Salut Mental i Addiccions, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Biomedical Network Research Centre on Mental Health (CIBERSAM), Barcelona, Catalonia, Spain. Departament de Psiquiatria i Medicina Legal, Universitat Autònoma de Barcelona, Bellaterra, Spain, Vall d'Hebron Barcelona Hospital Campus, Cognitive Psychology, IBBA, Clinical Neuropsychology, Interdisciplinary Centre Psychopathology and Emotion regulation (ICPE), Clinical Cognitive Neuropsychiatry Research Program (CCNP), Pediatric surgery, and Radiology and nuclear medicine
Subjects: Dominància cerebral, trastornos mentales::trastornos del desarrollo neurológico::trastornos generalizados del desarrollo del niño::trastorno del espectro del autismo [PSIQUIATRÍA Y PSICOLOGÍA], Autism Spectrum Disorder, Caudate nucleus, Attention-deficit, Audiology, sistema nervioso::sistema nervioso central::encéfalo [ANATOMÍA], 0302 clinical medicine, Mental Disorders::Neurodevelopmental Disorders::Attention Deficit and Disruptive Behavior Disorders::Attention Deficit Disorder with Hyperactivity [PSYCHIATRY AND PSYCHOLOGY], 130 000 Cognitive Neurology & Memory, Developmental and Educational Psychology, Brain asymmetry, Child, media_common, large-scale data, brain laterality, 05 social sciences, scale data, Brain, hyperactivity disorder, brain asymmetry, structural MRI, Mental Disorders::Neurodevelopmental Disorders::Child Development Disorders, Pervasive::Autism Spectrum Disorder [PSYCHIATRY AND PSYCHOLOGY], Magnetic Resonance Imaging, Psychiatry and Mental health, Globus pallidus, Attention&#8208, Autism spectrum disorder, Psychology, 050104 developmental & child psychology, Neuroinformatics, Adult, medicine.medical_specialty, Adolescent, media_common.quotation_subject, deficit, Nervous System::Central Nervous System::Brain [ANATOMY], Asymmetry, behavioral disciplines and activities, Article, 03 medical and health sciences, SDG 3 - Good Health and Well-being, Age groups, mental disorders, medicine, Humans, Attention deficit hyperactivity disorder, 0501 psychology and cognitive sciences, ddc:610, large&#8208, Other subheadings::Other subheadings::/diagnostic imaging [Other subheadings], Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], Otros calificadores::Otros calificadores::/diagnóstico por imagen [Otros calificadores], Cervell - Imatgeria, medicine.disease, Trastorn per dèficit d'atenció amb hiperactivitat, Attention Deficit Disorder with Hyperactivity, Pediatrics, Perinatology and Child Health, Orbitofrontal cortex, Caudate Nucleus, trastornos mentales::trastornos del desarrollo neurológico::trastornos conductuales disruptivos y déficit de atención::trastornos de déficit de atención con hiperactividad [PSIQUIATRÍA Y PSICOLOGÍA], 030217 neurology & neurosurgery
Abstract: Objective Some studies have suggested alterations of structural brain asymmetry in attention-deficit/hyperactivity disorder (ADHD), but findings have been contradictory and based on small samples. Here, we performed the largest ever analysis of brain left-right asymmetry in ADHD, using 39 datasets of the ENIGMA consortium. Methods We analyzed asymmetry of subcortical and cerebral cortical structures in up to 1,933 people with ADHD and 1,829 unaffected controls. Asymmetry Indexes (AIs) were calculated per participant for each bilaterally paired measure, and linear mixed effects modeling was applied separately in children, adolescents, adults, and the total sample, to test exhaustively for potential associations of ADHD with structural brain asymmetries. Results There was no evidence for altered caudate nucleus asymmetry in ADHD, in contrast to prior literature. In children, there was less rightward asymmetry of the total hemispheric surface area compared to controls (t = 2.1, p = .04). Lower rightward asymmetry of medial orbitofrontal cortex surface area in ADHD (t = 2.7, p = .01) was similar to a recent finding for autism spectrum disorder. There were also some differences in cortical thickness asymmetry across age groups. In adults with ADHD, globus pallidus asymmetry was altered compared to those without ADHD. However, all effects were small (Cohen’s d from −0.18 to 0.18) and would not survive study-wide correction for multiple testing. Conclusion Prior studies of altered structural brain asymmetry in ADHD were likely underpowered to detect the small effects reported here. Altered structural asymmetry is unlikely to provide a useful biomarker for ADHD, but may provide neurobiological insights into the trait., Journal of Child Psychology and Psychiatry, 62 (10), ISSN:0021-9630, ISSN:1469-7610
Published: 2021
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12. TWO SAMPLE UNIDIRECTIONAL MENDELIAN RANDOMIZATION ANALYSIS BETWEEN WHITE MATTER AND ADHD

Author: Maria de Araujo Tavares, Marina Xavier Carpena, Cibele Edom Bandeira, Renata Cupertino, Eduarda Colbeich da Silveira, Stefania Pigatto Teche, Eduardo S. Vitola, Eugênio H. Grevet, Diego Luiz Rovaris, Bruna Santos da Silva, and Claiton H.D. Bau
Subjects: Pharmacology, Psychiatry and Mental health, Neurology, Pharmacology (medical), Neurology (clinical), Biological Psychiatry
Published: 2022
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13. Systematic review and meta-analysis of the behavioral effects of methylphenidate in the spontaneously hypertensive rat model of attention-deficit/hyperactivity disorder

Author: Claiton H.D. Bau, Eugenio H. Grevet, Artur Alban Salvi, Diego L. Rovaris, Iraci Lucena da Silva Torres, Luis Augusto Rohde, Douglas Teixeira Leffa, Gabriel Natan Pires, and Alana Castro Panzenhagen
Subjects: Predictive validity, Cognitive Neuroscience, medicine.medical_treatment, Impulsivity, Behavioral Neuroscience, Spontaneously hypertensive rat, Memory, Rats, Inbred SHR, mental disorders, medicine, Animals, Attention deficit hyperactivity disorder, Attention, cardiovascular diseases, Behavior, Animal, Dose-Response Relationship, Drug, Methylphenidate, business.industry, Reproducibility of Results, Construct validity, medicine.disease, Stimulant, Disease Models, Animal, Neuropsychology and Physiological Psychology, Attention Deficit Disorder with Hyperactivity, Meta-analysis, Impulsive Behavior, cardiovascular system, Central Nervous System Stimulants, medicine.symptom, business, medicine.drug, Clinical psychology
Abstract: The spontaneously hypertensive rats (SHR) are the most widely used model for ADHD. While face and construct validity are consolidated, questions remain about the predictive validity of the SHR model. We aim at summarizing the evidence for the predictive validity of SHR by evaluating its ability to respond to methylphenidate (MPH), the most well documented treatment for ADHD. A systematic review was carried out to identify studies evaluating MPH effects on SHR behavior. Studies (n=36) were grouped into locomotion, attention, impulsivity or memory, and a meta-analysis was performed. Meta-regression, sensitivity, heterogeneity, and publication bias analyses were also conducted. MPH increased attentional and mnemonic performances in the SHR model and decreased impulsivity in a dose-dependent manner. However, MPH did not reduce hyperactivity in low and medium doses, while increased locomotor activity in high doses. Thus, since the paradoxical effect of stimulant in reducing hyperactivity was not observed in the SHR model, our study does not fully support the predictive validity of SHR, questioning their validity as an animal model for ADHD.
Published: 2019
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14. Revisiting ADHD age-of-onset in adults: to what extent should we rely on the recall of childhood symptoms?

Author: Eduardo S. Vitola, Claiton H.D. Bau, Luciana Anselmi, Eugenio H. Grevet, Luiz Rohde, Arthur Caye, Ana M. B. Menezes, Diego L. Rovaris, and Vitor Breda
Subjects: Adult, Male, Context (language use), Lower risk, Young Adult, mental disorders, medicine, Humans, Attention deficit hyperactivity disorder, Age of Onset, Applied Psychology, Male gender, Retrospective Studies, Recall, business.industry, Reproducibility of Results, medicine.disease, Mental health, Psychiatry and Mental health, Attention Deficit Disorder with Hyperactivity, Mental Recall, Structured interview, Regression Analysis, Female, Self Report, Age of onset, business, Brazil, Clinical psychology
Abstract: BackgroundADHD diagnosis requires the presence of symptoms before the age of twelve. In clinical assessment of adults, the most frequent strategy to check this criterion is investigating self-report recall of symptoms, despite little evidence on the validity of this approach. We aim to evaluate the recall accuracy and factors associated with its reliability in a large population-based sample of adults.MethodsIndividuals from the 1993 Pelotas Birth Cohort were followed-up from childhood to adulthood. At the age of 22, 3810 individuals were assessed through structured interviews by trained psychologists regarding mental health outcomes, including ADHD diagnosis and ADHD symptoms in childhood. The retrospective recall was compared with available information on ADHD childhood symptoms at the age of eleven. We also assessed factors related to recall accuracy through multiple regression analyses.ResultsSelf-reported recall of childhood symptoms at 22 years of age had an accuracy of only 55.4%, with sensitivity of 32.8% and positive predictive value of 40.7%. Current inattention symptoms were associated with lower risk and social phobia with higher risk for false-positive endorsement, while higher levels of schooling correlated with lower risk and male gender with higher risk for false-negative endorsement.ConclusionsClinicians treating male patients with social phobia and ADHD symptoms should assess even more carefully retrospective recall of ADHD childhood symptoms. Moreover, characteristics associated with recall improvement do not impact accuracy robustly. In this context, the recall of childhood ADHD symptoms seems an unreliable method to characterize the neurodevelopmental trajectory in adults with currently-impairing ADHD symptomatology.
Published: 2019
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15. Caffeine-related genes influence anxiety disorders in children and adults with ADHD

Author: Diego L. Rovaris, Verônica Contini, Eugenio H. Grevet, Cibele Edom Bandeira, Luis Augusto Rohde, Julia P. Genro, Bruna Santos da Silva, Fabiane Dresch, Claiton H.D. Bau, Mara H. Hutz, Luciana Tovo-Rodrigues, Thailan Teles Fraporti, and Thais Martins-Silva
Subjects: Adult, Genome-wide association study, Comorbidity, Anxiety, chemistry.chemical_compound, Caffeine, mental disorders, medicine, Attention deficit hyperactivity disorder, Humans, Biological Psychiatry, business.industry, Central nervous system stimulant, medicine.disease, Anxiety Disorders, Psychiatry and Mental health, Alertness, chemistry, Attention Deficit Disorder with Hyperactivity, Etiology, Central Nervous System Stimulants, medicine.symptom, business, Anxiety disorder, Clinical psychology
Abstract: Attention-deficit/hyperactivity disorder (ADHD) and anxiety disorders (AD) frequently co-occur, increasing morbidity and challenging treatment. Caffeine is a central nervous system stimulant and acts in the brain through adenosine receptors, influencing attention, alertness, and anxiety. In the present study, we performed a gene-set analysis to verify if genes related to caffeine response are associated with anxiety disorders in 240 children and 406 adults with ADHD. We demonstrated an association between the gene-set with AD in children (P = 0.0054) and with the number of anxiety disorders in adults (P = 0.0197). In order to test if this effect is a result of anxiety in general or is related to AD comorbid with ADHD, we evaluated the association between caffeine gene-set with AD in an adult control sample. The gene-set was neither associated with the AD presence (P = 0.3008) nor with the number of AD (P = 0.5594) in this control sample. We also test this gene set with ADHD (n = 55,374) and AD (n = 18,186) GWAS summary statistics, and we did not observe significant results with ADHD (P = 0.5587) or AD (P = 0.3930). These findings suggest the caffeine-related genes play a role in the etiology of an anxiety disorder phenotype present in children and adults with ADHD.
Published: 2021

16. Attention-deficit/hyperactivity disorder has a state-dependent association with asthma: The role of systemic inflammation in a population-based birth cohort followed from childhood to adulthood

Author: Eduardo S. Vitola, Arthur Caye, Fernando C. Wehrmeister, Iná S. Santos, Eugenio H. Grevet, Isabel O. Oliveira, Douglas Teixeira Leffa, Luis Augusto Rohde, Claiton H.D. Bau, Luciana Tovo-Rodrigues, Ana M. B. Menezes, and Alicia Matijasevich
Subjects: Pediatrics, medicine.medical_specialty, Adolescent, Immunology, Comorbidity, Systemic inflammation, Behavioral Neuroscience, Young Adult, mental disorders, medicine, Attention deficit hyperactivity disorder, Humans, Child, Asthma, Inflammation, biology, Endocrine and Autonomic Systems, business.industry, Incidence (epidemiology), C-reactive protein, Confounding, Infant, Newborn, medicine.disease, Cross-Sectional Studies, Attention Deficit Disorder with Hyperactivity, Cohort, biology.protein, medicine.symptom, business
Abstract: There is a high comorbidity between attention-deficit/hyperactivity disorder (ADHD) and asthma, and inflammation has been proposed as a potential pathophysiological mechanism behind this association. Most studies conducted so far have used a cross-sectional design, and none has evaluated the prevalence of asthma symptoms in patients with ADHD followed from childhood to adulthood. We relied on data from the 1993 Pelotas birth cohort to evaluate the association between ADHD and asthma in patients with distinct patterns of incidence, persistence and remission, and to explore the potential role of inflammatory markers in the comorbidity. We analyzed data from 3281 individuals from the 1993 Pelotas birth cohort collected at birth (1993), 11 years (2004), 18 years (2011), and 22 years (2015). Subjects were first classified according to their ADHD and asthma status as early-onset (EO) persistent (positive screening for ADHD at 11 years and diagnosis of ADHD according to DSM-5, except criterion E, at either 18 or 22 years), EO-remittent (positive screening for ADHD at 11 years only), late-onset (diagnosis of ADHD according to DSM-5, except criterion E, at 18 or 22 years only), or healthy subjects (negative for both conditions in all evaluation). After controlling for confounders, significant associations were observed between EO-remittent ADHD and EO-remittent asthma (OR 1.68, 95% CI 1.11–2.55), EO-persistent ADHD and EO-persistent asthma (OR 4.33, 95% CI 1.65–11.34), and between late-onset ADHD and late-onset asthma (OR 1.86, 95% CI 1.28–2.70), suggesting a state-dependent association. Serum interleukin-6 (IL-6) and C-reactive protein (CRP) were measured at the 18- and 22-year evaluations and compared between subjects positive for ADHD, asthma, and subjects with both or none conditions, regardless of the previously defined trajectories. Subjects with comorbid ADHD and asthma presented higher levels of IL-6 at the 18- and 22-year evaluations when compared to subjects negative for both conditions. Our results demonstrate a state-dependent association between ADHD and asthma despite underlying trajectories. Higher levels of serum IL-6 in patients with both conditions suggest that a pro-inflammatory environment might have a role in the pathophysiological mechanisms underlying the comorbidity.
Published: 2021

17. W1. CHARACTERIZING FOXP2 EFFECTS ON CLINICAL PHENOTYPES IN ADULTS WITH ADHD

Author: Maria Eduarda Tavares, Stefania Pigatto Teche, Renata B. Cupertino, Diego L. Rovaris, Claiton H.D. Bau, Luis Augusto Rohde, Eduarda Pereira Oliveira, Bruna Santos da Silva, Cibele Edom Bandeira, Diana Müller, Gabriela P. Meyer, Eugenio H. Grevet, and Robson dos Santos Soares
Subjects: Pharmacology, Genetics, Psychiatry and Mental health, Neurology, Pharmacology (medical), FOXP2, Neurology (clinical), Biology, Phenotype, Biological Psychiatry
Published: 2021
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18. TH2. CAFFEINE-RELATED GENES INFLUENCE ANXIETY DISORDERS IN CHILDREN AND ADULTS WITH ADHD

Author: Eugenio H. Grevet, Thais Martins-Silva, Julia P. Genro, Bruna Santos da Silva, Thailan Teles Fraporti, Veônica Contini, Luciana Tovo-Rodrigues, Luis Augusto Rohde, Fabiane Dresch, Diego L. Rovaris, Mara H. Hutz, Claiton H.D. Bau, and Cibele Edom Bandeira
Subjects: Pharmacology, business.industry, Psychiatry and Mental health, chemistry.chemical_compound, Neurology, chemistry, medicine, Anxiety, Pharmacology (medical), Neurology (clinical), medicine.symptom, Caffeine, business, Gene, Biological Psychiatry, Clinical psychology
Published: 2021
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19. Expanding the discussion on experimental models of attention deficit hyperactivity disorder

Author: Alana C. Panzenhagen, Claiton H.D. Bau, Eugenio H. Grevet, and Diego L. Rovaris
Subjects: Behavioral Neuroscience, Neuropsychology and Physiological Psychology, Cognitive Neuroscience
Published: 2022
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20. The neurodevelopmental nature of attention-deficit hyperactivity disorder in adults

Author: Vitor Breda, Diego L. Rovaris, Arthur Caye, Luciana Anselmi, Ana M. B. Menezes, Luis Augusto Rohde, Claiton H.D. Bau, Eduardo S. Vitola, and Eugenio H. Grevet
Subjects: Adult, Male, Adolescent, Population, Late onset, Late Onset Disorders, 03 medical and health sciences, Young Adult, 0302 clinical medicine, Neurodevelopmental disorder, Medicine, Attention deficit hyperactivity disorder, Humans, Longitudinal Studies, Age of Onset, education, Child, education.field_of_study, business.industry, medicine.disease, 030227 psychiatry, Psychiatry and Mental health, Attention Deficit Disorder with Hyperactivity, Neurodevelopmental Disorders, Female, business, Birth cohort, 030217 neurology & neurosurgery, Clinical psychology
Abstract: BackgroundPopulation studies have suggested that most adults with attention-deficit hyperactivity disorder (ADHD) did not have the disorder in childhood, challenging the neurodevelopmental conceptualisation of ADHD. Arbitrary definitions of age at onset and lack of defined trajectories were accounted for the findings.AimsThe objective of this study was to assess the proportion of individuals presenting with either a neurodevelopmental trajectory or late-onset disorder, and to assess risk factors associated with them.MethodData of 4676 individuals from the 1993 Pelotas birth cohort at 11, 15, 18 and 22 years of age were used. Polythetic and latent class mixed model analyses were performed to define ADHD trajectories from childhood to adulthood, and characterise the neurodevelopmental or late-onset courses. Regression models were applied to assess factors associated with different trajectories.ResultsClassical polythetic analyses showed that 67% of those with ADHD at 22 years of age had a neurodevelopmental course of the disorder. Latent class mixed model analysis indicated that 78% of adults with ADHD had a trajectory of persistent symptoms, more common in males. The remaining adults with ADHD had an ascending symptom trajectory that occurred after puberty, with late-onset ADHD associated with female gender and higher IQ.ConclusionsBoth polythetic and latent trajectories analyses provided empirical evidence supporting that the large majority of adults with ADHD had a neurodevelopmental disorder.
Published: 2020

21. Feasibility trial of the dialectical behavior therapy skills training group as add-on treatment for adults with attention-deficit/hyperactivity disorder

Author: Mariana S. Dillenburg, Michel M. P. Andreola, Patrícia Basso, Leandro Timm Pizutti, Guilherme R. Moritz, Laura B. Lewgoy, Ana Carolina Macie Cancian, Lucas André Schuster de Souza, Luis Augusto Rohde, Eugenio H. Grevet, Marcelo M. Victor, Claiton H.D. Bau, Stefania Pigatto Teche, and Alexandra Philipsen
Subjects: Adult, Male, 050103 clinical psychology, medicine.medical_specialty, medicine.medical_treatment, Dialectical Behavior Therapy, law.invention, Group psychotherapy, 03 medical and health sciences, Skills training, 0302 clinical medicine, Arts and Humanities (miscellaneous), Randomized controlled trial, law, Completion rate, mental disorders, medicine, Attention deficit hyperactivity disorder, Humans, 0501 psychology and cognitive sciences, 05 social sciences, Attendance, medicine.disease, Dialectical behavior therapy, 030227 psychiatry, Clinical trial, Clinical Psychology, Treatment Outcome, Attention Deficit Disorder with Hyperactivity, Physical therapy, Feasibility Studies, Female, Psychology
Abstract: OBJECTIVE Our aim was to explore the feasibility, and efficacy of a Dialectical Behavior Therapy Skill Training Group (DBT-ST) as an add-on treatment for adult attention-deficit/hyperactivity disorder (ADHD) in Latin America. METHOD Adults with ADHD (n = 31) with stable medication treatment for ADHD and residual symptoms (ASRS > 20) were randomly assigned to DBT-ST (n = 16) or treatment as usual (TaU; n = 15) for 12 weeks. Feasibility was accessed by attendance and completion rates at 12 weeks. Efficacy outcomes were measured with the ASRS, and performed at 0, 6, 12, and 16 weeks. RESULTS The DBT-ST protocol had 81.25% completion rate, with a mean attendance of 87.25% of the sessions. No significant interactions between group and time were detected for outcome measures. DISCUSSION The DBT-ST was feasible as add-on treatment for adult patients with ADHD in Latin America. Replicating previous findings, DBT-ST has shown no significantly higher improvement in ADHD symptoms in comparison with TaU. Registered at the Clinical Trials database (NCT03326427).
Published: 2020

22. Reduced fronto-striatal volume in attention-deficit/hyperactivity disorder in two cohorts across the lifespan

Author: Marcel P. Zwiers, Eduardo S. Vitola, Vitor Breda, Diego L. Rovaris, Pieter J. Hoekstra, Catharina A. Hartman, Barbara Franke, Felipe Almeida Picon, Sourena Soheili-Nezhad, Renata B. Cupertino, Christian F. Beckmann, Cibele Edom Bandeira, Jilly Naaijen, Claiton H.D. Bau, Jaap Oosterlaan, Daan van Rooij, Maria Eduarda Tavares, Sophie E.A. Akkermans, Jan K. Buitelaar, Emma Sprooten, Eugenio H. Grevet, Clinical Cognitive Neuropsychiatry Research Program (CCNP), General Paediatrics, ARD - Amsterdam Reproduction and Development, Pediatric surgery, Clinical Neuropsychology, IBBA, and APH - Mental Health
Subjects: CHILDREN, Audiology, lcsh:RC346-429, 0302 clinical medicine, MATTER ABNORMALITIES, 130 000 Cognitive Neurology & Memory, Gray Matter, Child, 05 social sciences, White matter, 220 Statistical Imaging Neuroscience, Brain, Regular Article, Magnetic Resonance Imaging, medicine.anatomical_structure, Neurology, VOXEL-BASED MORPHOMETRY, Cohort, lcsh:R858-859.7, Brazil, Adult, medicine.medical_specialty, DEFICIT HYPERACTIVITY DISORDER, Cognitive Neuroscience, Longevity, Independent component analysis, lcsh:Computer applications to medicine. Medical informatics, behavioral disciplines and activities, 050105 experimental psychology, 150 000 MR Techniques in Brain Function, 03 medical and health sciences, Brain anatomy, Neuroimaging, mental disorders, medicine, Attention deficit hyperactivity disorder, Humans, ADHD, 0501 psychology and cognitive sciences, Radiology, Nuclear Medicine and imaging, Association (psychology), lcsh:Neurology. Diseases of the nervous system, METAANALYSIS, GRAY, Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], INDEPENDENT COMPONENT ANALYSIS, business.industry, Fronto-striatal, Tensor-based morphometry, ADULTS, medicine.disease, Attention Deficit Disorder with Hyperactivity, Neurology (clinical), PSYCHIATRIC COMORBIDITY, business, 030217 neurology & neurosurgery
Abstract: Highlights • Reduced volume in frontal lobes, striatum, and their interconnecting white matter in ADHD. • Cross-cultural and age-independent validity of the study including two independent cohorts. • Data driven approach using ICA of whole-brain morphometry images., Attention-Deficit/Hyperactivity Disorder (ADHD) has been associated with altered brain anatomy in neuroimaging studies. However, small and heterogeneous study samples, and the use of region-of-interest and tissue-specific analyses have limited the consistency and replicability of these effects. We used a data-driven multivariate approach to investigate neuroanatomical features associated with ADHD in two independent cohorts: the Dutch NeuroIMAGE cohort (n = 890, 17.2 years) and the Brazilian IMpACT cohort (n = 180, 44.2 years). Using independent component analysis of whole-brain morphometry images, 375 neuroanatomical components were assessed for association with ADHD. In both discovery (corrected-p = 0.0085) and replication (p = 0.032) cohorts, ADHD was associated with reduced volume in frontal lobes, striatum, and their interconnecting white-matter. Current results provide further evidence for the role of the fronto-striatal circuit in ADHD in children, and for the first time show its relevance to ADHD in adults. The fact that the cohorts are from different continents and comprise different age ranges highlights the robustness of the findings.
Published: 2020
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23. Effects of DRD2 splicing-regulatory polymorphism and DRD4 48 bp VNTR on crack cocaine addiction

Author: Diana Müller, Diego L. Rovaris, Claiton H.D. Bau, Eugenio H. Grevet, Jaqueline Bohrer Schuch, Renata B. Cupertino, Tatiana Roman, Eduardo S. Vitola, Anderson Ravy Stolf, Lisia von Diemen, Flavio Pechansky, Breno Sanvicente-Vieira, Felix Kessler, and Rodrigo Grassi-Oliveira
Subjects: Adult, Male, 0301 basic medicine, medicine.medical_specialty, media_common.quotation_subject, Minisatellite Repeats, Cocaine-Related Disorders, Young Adult, 03 medical and health sciences, Exon, Sex Factors, 0302 clinical medicine, Internal medicine, Dopamine receptor D2, mental disorders, medicine, Dopamine receptor D4, Humans, Genetic Predisposition to Disease, Allele, Biological Psychiatry, media_common, Polymorphism, Genetic, biology, Receptors, Dopamine D2, business.industry, Addiction, Receptors, Dopamine D4, Dopaminergic, medicine.disease, Substance abuse, Psychiatry and Mental health, Cross-Sectional Studies, 030104 developmental biology, Endocrinology, Neurology, Dopamine receptor, biology.protein, Crack Cocaine, Female, Neurology (clinical), business, 030217 neurology & neurosurgery
Abstract: There is evidence that dopamine receptors D2 (DRD2) and D4 (DRD4) polymorphisms may influence substance use disorders (SUD) susceptibility both individually and through their influence in the formation of DRD2-DRD4 heteromers. The dopaminergic role on the vulnerability to addiction appears to be influenced by sex. A cross-sectional study with 307 crack cocaine addicts and 770 controls was conducted. The influence of DRD2 rs2283265 and DRD4 48 bp VNTR in exon 3 variants, as well as their interaction on crack cocaine addiction susceptibility and severity were evaluated in women and men separately. An association between the DRD2 T allele and crack cocaine addiction was found in women. In this same group, interaction analysis demonstrated that the presence of DRD2-T allele and concomitant absence of DRD4-7R allele were associated with risk for crack cocaine addiction. No influence of DRD2 and DRD4 variants was observed in men regarding addiction severity. This study reinforces the role of dopaminergic genes in externalizing behaviors, especially the influence of DRD2-DRD4 interaction on SUD. This is the fourth sample that independently associated the DRD2-DRD4 interaction with SUD itself or related disorders. In addition, our findings point out to a potential difference of dopaminergic neurotransmission across sex influencing addiction susceptibility.
Published: 2018
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24. Exploring neuropsychological predictors of ADHD remission or persistence during adulthood

Author: Diego L. Rovaris, Rafael G. Karam, Eugenio H. Grevet, Luis Augusto Rohde, Claiton H.D. Bau, Paula O. Guimarães-da-Silva, and Katiane L. Silva
Subjects: Adult, Male, Persistence (psychology), Cognitive Neuroscience, Remission, Spontaneous, education, Neuropsychological Tests, Impulsivity, 03 medical and health sciences, 0302 clinical medicine, mental disorders, medicine, Humans, Attention deficit hyperactivity disorder, Child, Neuropsychology, Follow up studies, Cognition, Prognosis, medicine.disease, 030227 psychiatry, Psychiatry and Mental health, Neuropsychiatric disorder, Attention Deficit Disorder with Hyperactivity, Female, medicine.symptom, Psychology, psychological phenomena and processes, 030217 neurology & neurosurgery, Follow-Up Studies, Clinical psychology
Abstract: Attention Deficit Hyperactivity Disorder (ADHD) is a neuropsychiatric disorder characterized by symptoms of inattention, hyperactivity and impulsivity (APA, 2013) with a prevalence of 5.3% in child...
Published: 2018
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25. Searching for ancient balanced polymorphisms shared between Neanderthals and Modern Humans

Author: Claiton H.D. Bau, Maria Cátira Bortolini, Carlos Eduardo G. Amorim, David Comas, Vanessa Rodrigues Paixão-Côrtes, Lucas Henriques Viscardi, Diego L. Rovaris, and Francisco M. Salzano
Subjects: 0301 basic medicine, immune genes, lcsh:QH426-470, behavioral genes, balancing selection, Human behavior, Archaic humans, Single-nucleotide polymorphism, Balancing selection, 03 medical and health sciences, 0302 clinical medicine, evolution, Genetics, Molecular Biology, Denisovan, Exome sequencing, biology, Repertoire, biology.organism_classification, lcsh:Genetics, 030104 developmental biology, Human evolution, Homo sapiens, Evolutionary biology, Human and Medical Genetics, 030217 neurology & neurosurgery
Abstract: Hominin evolution is characterized by adaptive solutions often rooted in behavioral and cognitive changes. If balancing selection had an important and long-lasting impact on the evolution of these traits, it can be hypothesized that genes associated with them should carry an excess of shared polymorphisms (trans- SNPs) across recent Homo species. In this study, we investigate the role of balancing selection in human evolution using available exomes from modern (Homo sapiens) and archaic humans (H. neanderthalensis and Denisovan) for an excess of trans-SNP in two gene sets: one associated with the immune system (IMMS) and another one with behavioral system (BEHS). We identified a significant excess of trans-SNPs in IMMS (N=547), of which six of these located within genes previously associated with schizophrenia. No excess of trans-SNPs was found in BEHS, but five genes in this system harbor potential signals for balancing selection and are associated with psychiatric or neurodevelopmental disorders. Our approach evidenced recent Homo trans-SNPs that have been previously implicated in psychiatric diseases such as schizophrenia, suggesting that a genetic repertoire common to the immune and behavioral systems could have been maintained by balancing selection starting before the split between archaic and modern humans.
Published: 2018

26. EPIGENETICS OF COCAINE USE DISORDER IN SOUTHERN BRAZIL

Author: Thiago Wendt Viola, Claiton H.D. Bau, Diego L. Rovaris, Rodrigo Grassi-Oliveira, Consuelo Walss-Bass, Gabriel Rodrigo Fries, Zhongming Zhao, Laura Stertz, Joy M. Schmitz, and Eugenio H. Grevet
Subjects: Pharmacology, Psychiatry and Mental health, medicine.medical_specialty, Neurology, business.industry, medicine, Cocaine use, Pharmacology (medical), Neurology (clinical), Epigenetics, Psychiatry, business, Biological Psychiatry
Published: 2021
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27. TH65. POLYGENIC RISK SCORES FOR ADHD AND TREATMENT RESPONSE TO METHYLPHENIDATE

Author: Cibele Edom Bandeira, Maria Eduarda Tavares, Pâmela Ferreira da Cunha, Guilherme Machado, Diego L. Rovaris, Marcelo Vitor, Eugenio H. Grevet, Claiton H.D. Bau, and Bruna Santos da Silva
Subjects: Pharmacology, Oncology, Treatment response, medicine.medical_specialty, Methylphenidate, business.industry, Psychiatry and Mental health, Neurology, Internal medicine, medicine, Pharmacology (medical), Polygenic risk score, Neurology (clinical), business, Biological Psychiatry, medicine.drug
Published: 2021
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28. TH52. REFINING PATTERNS OF MEF2C ASSOCIATIONS WITH WHITE MATTER MICROSTRUCTURE AND PSYCHIATRIC FEATURES

Author: Claiton H.D. Bau, Eduardo S. Vitola, Eugenio H. Grevet, Robson dos Santos Soares, Renata B. Cupertino, Maria de Araujo Tavares, Cibele Edom Bandeira, Felipe Almeida Picon, Bruna Santos da Silva, Carlos A.I. Salgado, and Diego L. Rovaris
Subjects: Pharmacology, Psychiatry and Mental health, Neurology, Pharmacology (medical), Neurology (clinical), Psychology, White matter microstructure, Biological Psychiatry, Clinical psychology, Refining (metallurgy)
Published: 2021
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29. TU1. POLYGENIC RISK SCORE ANALYSES FOR ATTENTION-DEFICIT/HYPERACTIVITY DISORDER TRAJECTORIES IN ADULTS

Author: Maria Eduarda Tavares, Stefania Pigatto Teche, Claiton H.D. Bau, Renata B. Cupertino, Vitor Breda, Eduardo S. Vitola, Luis Augusto Rohde, Diego L. Rovaris, Eugenio H. Grevet, Cibele Edom Bandeira, Gregory Zeni, Felipe Almeida Picon, and Bruna Santos da Silva
Subjects: Pharmacology, Psychiatry and Mental health, Neurology, business.industry, Medicine, Attention deficit hyperactivity disorder, Pharmacology (medical), Polygenic risk score, Neurology (clinical), business, medicine.disease, Biological Psychiatry, Clinical psychology
Published: 2021
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30. Further replication of the synergistic interaction between LPHN3 and the NTAD gene cluster on ADHD and its clinical course throughout adulthood

Author: Diego L. Rovaris, Eugenio H. Grevet, Eduardo S. Vitola, Bruna Santos da Silva, Stefania Pigatto Teche, Renata B. Cupertino, Luis Augusto Rohde, Nina Roth Mota, Jaqueline Bohrer Schuch, Claiton H.D. Bau, Rafael G. Karam, Cristina Winkler, and Djenifer B. Kappel
Subjects: Adult, Male, 0301 basic medicine, Receptors, Peptide, Single-nucleotide polymorphism, Protein Serine-Threonine Kinases, Impulsivity, Polymorphism, Single Nucleotide, Receptors, G-Protein-Coupled, 03 medical and health sciences, 0302 clinical medicine, mental disorders, Gene cluster, Genotype, medicine, Humans, Genetic Predisposition to Disease, Allele, Gene, Biological Psychiatry, Retrospective Studies, Pharmacology, Genetics, Receptors, Dopamine D2, Proteins, Heritability, Phenotype, CD56 Antigen, 030104 developmental biology, Attention Deficit Disorder with Hyperactivity, Multigene Family, Disease Progression, Female, medicine.symptom, Psychology, 030217 neurology & neurosurgery, Follow-Up Studies
Abstract: Attention-Deficit/Hyperactivity Disorder (ADHD) is a common and highly heritable neuropsychiatric disorder. Despite the high heritability, the unraveling of specific genetic factors related to ADHD is hampered by its considerable genetic complexity. Recent evidence suggests that gene-gene interactions can explain part of this complexity. We examined the impact of strongly supported interaction effects between the LPHN3 gene and the NTAD gene cluster (NCAM1-TTC12-ANKK1-DRD2) in a 7-year follow-up of a clinical sample of adults with ADHD, addressing associations with susceptibility, symptomatology and stability of diagnosis. The sample comprises 548 adults with ADHD and 643 controls. Entropy-based analysis indicated a potential interaction between the LPHN3-rs6551665 and TTC12-rs2303380 SNPs influencing ADHD symptom counts. Further analyses revealed significant interaction effects on ADHD total symptoms (p=0.002), and with hyperactivity/impulsivity symptom counts (p=0.005). In the group composed by predominantly hyperactive/impulsive and combined presentation, the presence of LPHN3-rs6551665 G allele was related to increased ADHD risk only in individuals carrying the TTC12-rs2303380 AA genotype (p=0.026). Also, the same allelic constellation is involved in maintenance of ADHD in a predominantly hyperactive/impulsive or combined presentation after a 7-year follow-up (p=0.008). These observations reinforce and replicate previous evidence suggesting that an interaction effect between the LPHN3 gene and the NTAD cluster may have a role in the genetic substrate associated to ADHD also in adults. Moreover, it is possible that the interactions between LPHN3 and NTAD are specific factors contributing to the development of an ADHD phenotype with increased hyperactivity/impulsivity that is maintained throughout adulthood.
Published: 2017
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31. Exocytosis-related genes and response to methylphenidate treatment in adults with ADHD

Author: Claiton H.D. Bau, Diana Müller, Verônica Contini, Rafael G. Karam, Marcelo M. Victor, Nina Roth Mota, Cibele Edom Bandeira, B S da Silva, Eugenio H. Grevet, Djenifer B. Kappel, Jaqueline Bohrer Schuch, Renata B. Cupertino, Luiz Rohde, and Diego L. Rovaris
Subjects: Adult, Male, Oncology, medicine.medical_specialty, Vesicle-Associated Membrane Protein 2, Syntaxin 1, Exocytosis, 03 medical and health sciences, Cellular and Molecular Neuroscience, All institutes and research themes of the Radboud University Medical Center, 0302 clinical medicine, Rating scale, Internal medicine, Outcome Assessment, Health Care, mental disorders, medicine, Humans, Molecular Biology, Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], Polymorphism, Genetic, STX1A, Methylphenidate, medicine.disease, 030227 psychiatry, Psychiatry and Mental health, Treatment Outcome, Attention Deficit Disorder with Hyperactivity, Attention Deficit and Disruptive Behavior Disorders, Schizophrenia, Synaptotagmin I, Pharmacodynamics, Behavioral medicine, Central Nervous System Stimulants, Female, Psychopharmacology, Psychology, 030217 neurology & neurosurgery, Pharmacogenetics, Clinical psychology, medicine.drug
Abstract: Experimental studies have demonstrated that methylphenidate (MPH) modulates the synaptic vesicle trafficking and synaptotagmin-1 (SytI) mRNA levels. SytI is a regulatory protein of the SNARE complex, a neurotransmitter exocytosis mediator. Despite this evidence, most SNARE complex-related genes have never been evaluated in attention-deficit/hyperactivity disorder (ADHD) pharmacogenetics. This study evaluates, for we believe the first time, polymorphisms on the SNARE complex-related genes STX1A (rs2228607), VAMP2 (26bp Ins/Del) and SYT1 (rs1880867 and rs2251214) on the response to immediate-release methylphenidate (IR-MPH) in a naturalistic sample of adults with ADHD. The sample comprised 433 subjects, of which 272 (62.8%) have completed the short-term IR-MPH treatment (at least 30 days). The main outcome measure was the categorical variable of short-term response to IR-MPH based on the Swanson, Nolan and Pelham Rating Scale version 4 (SNAP-IV), and on the clinical global impression-improvement scale. Additional analyses evaluated the percentage of SNAP-IV symptom reduction for each dimension as well as short- and long- (7 years) term treatment persistence. SYT1-rs2251214 was associated with the categorical short-term response to IR-MPH (P=0.006, PFDR=0.028), and with the percentage of inattention and oppositional defiant disorder symptoms reduction (P=0.007, PFDR=0.028 and P=0.017, PFDR=0.048, respectively). SYT1-rs2251214 was also associated with short-term treatment persistence (P=0.018, PFDR=0.048), and with months of treatment (P=0.002, PFDR=0.016) in the long-term protocol. Our findings suggest that SYT1-rs2251214 presents a broad influence in IR-MPH response variability in adults with ADHD, being involved with both symptom response and treatment persistence. If such findings are replicated, SytI could represent a key element in MPH pharmacodynamics in adults with ADHD.
Published: 2017
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32. The Role of Gene Encoding Variation ofDRD4in the Relationship between Inattention and Seasonal Daylight

Author: Josep Antoni Ramos-Quiroga, Jonna Kuntsi, Arvid Lundervold, Cristina Sánchez-Mora, Eugenio H. Grevet, Jan Haavik, L.E. Arnold, Barbara Franke, Marta Ribasés, Martijn Arns, Sandra K. Loo, James M. Swanson, Madelon A. Vollebregt, Andreas Reif, P. Asherson, Janita Bralten, Claiton H.D. Bau, Stephen V. Faraone, Tetyana Zayats, Jan K. Buitelaar, and Renata B. Cupertino
Subjects: Sunlight, 0303 health sciences, Physiology, Independent measure, Cognition, Biology, 03 medical and health sciences, 0302 clinical medicine, Variation (linguistics), Dopamine, Genetic variation, medicine, Daylight, Circadian rhythm, 030217 neurology & neurosurgery, 030304 developmental biology, medicine.drug
Abstract: Daylight is the strongest synchronizer of human circadian rhythms. The circadian pathway hypothesis posits that synchrony between daylight and the circadian system relates to (in)attention. The dopamine neurotransmitter system is implicated in regulating the circadian system as well as in (attention)-deficit hyperactivity disorder [ADHD]. We studied the role of functional genetic variation in the gene encoding of dopamine-receptor-D4 (DRD4) in the relationship between inattention and seasonal daylight (changes). Gene-by-environment (GxE) mega-analyses were performed across eight studies including 3757 adult participants (with and without ADHD). We tested 1) theSpring-focus hypothesis, in which attention in 7R-carriers normalizes with increasing daylight levels preceding measurement, 2) theSummer-born ADHD hypothesis, in which 7R-carriers report more inattention when born in spring/summer than in autumn/winter, 3) theWinter-born ADHD hypothesis, opposing the second hypothesis. TheSpring-focus hypothesiswas upheld (1386 ADHD, 760 controls;d=-0.16 between periods); 7R-carriers reported evenlessinattention than 7R-non-carriers after winter solstice (d=0.27 between genotype-groups). Results were diagnosis-independent. Sensitivity analyses at individual study level confirmed the circannual patterns for 7R-carriers. Incorporating geographic changes into the independent measure, we also calculated changes in sunlight levels. This approach likewise showed that inattention correlated negatively with increasing light levels in 7R-carriers (r=-.135). Results emphasize peripheral effects of dopamine and the effects of (seasonal) daylight changes on cognition.
Published: 2019
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33. Reduced fronto-striatal volume in ADHD in two cohorts across the lifespan

Author: Jilly Naaijen, Sourena Soheili-Nezhad, Renata B. Cupertino, Maria Eduarda Tavares, Vitor Breda, Barbara Franke, Eduardo S. Vitola, Marcel P. Zwiers, Felipe Almeida Picon, Jan K. Buitelaar, Catharina A. Hartman, Christian F. Beckmann, Jaap Oosterlaan, Claiton H.D. Bau, Daan van Rooij, Cibele Edom Bandeira, Sophie E.A. Akkermans, Pieter J. Hoekstra, Eugenio H. Grevet, and Emma Sprooten
Subjects: medicine.medical_specialty, Multivariate statistics, business.industry, Audiology, Cross-validation, 030227 psychiatry, White matter, 03 medical and health sciences, Brain anatomy, 0302 clinical medicine, medicine.anatomical_structure, Neuroimaging, Cohort, Brain size, medicine, Orbitofrontal cortex, business, 030217 neurology & neurosurgery
Abstract: ObjectiveNeuroimaging studies have associated Attention-Deficit/Hyperactivity Disorder (ADHD) with altered brain anatomy. However, small and heterogeneous study samples, and the use of region-of-interest and tissue-specific analyses have limited the consistency and replicability of these effects. The present study uses a fully data-driven multivariate approach to investigate alterations in both gray and white matter simultaneously, and capture neuroanatomical features associated with ADHD in two large, independent, demographically different cohorts.MethodsThe study comprised two ADHD cohorts with structural magnetic resonance imaging data: the Dutch NeuroIMAGE cohort (n=890, average age 17.2 years, discovery sample) and the Brazilian IMpACT cohort (n=180, average age 44.2 years, cross validation sample). Using independent component analysis of whole-brain morphometry images in the NeuroIMAGE cohort, 375 independent components of neuroanatomical variations were extracted and assessed their association with ADHD. Afterwards, ADHD-associated components were cross validated in the Brazilian IMpACT cohort.ResultsIn both discovery (corrected-p=0.020) and validation (p=0.033) cohorts, ADHD diagnosis was significantly associated with reduced brain volume in a component mapping to frontal lobes, striatum, and their interconnecting white-matter tracts. The most pronounced case-control differences were localized in white matter adjacent to the orbitofrontal cortex.ConclusionIndependent component analysis is a sensitive approach to uncover neuroanatomical alterations in ADHD and avoid bias attributable toa prioriregion-of-interest based methods. Current results provide further evidence for the role of the fronto-striatal circuit in ADHD. The fact that the two cohorts are from different continents and comprising different age ranges highlights the robustness of the findings.
Published: 2019
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34. Association between cognitive performance and SYT1-rs2251214 among women with cocaine use disorder

Author: Aline Zaparte, Diego L. Rovaris, Rodrigo Grassi-Oliveira, Lucca Pizzato Tondo, Thiago Wendt Viola, Bruna Santos da Silva, Renata B. Cupertino, Rafael Genovese, Claiton H.D. Bau, Jaqueline Bohrer Schuch, and Breno Sanvicente-Vieira
Subjects: 0301 basic medicine, Adult, medicine.medical_specialty, Neurology, SYT1, Polymorphism, Single Nucleotide, Article, 03 medical and health sciences, Cocaine-Related Disorders, 0302 clinical medicine, SNP, Medicine, Humans, Cognitive Dysfunction, Effects of sleep deprivation on cognitive performance, Association (psychology), Biological Psychiatry, business.industry, Cognition, Psychiatry and Mental health, 030104 developmental biology, Cross-Sectional Studies, Case-Control Studies, Synaptotagmin I, Cocaine use, Female, Neurology (clinical), business, 030217 neurology & neurosurgery, Clinical psychology, Stroop effect
Abstract: The SNP rs2251214 of the SYT1 gene was recently associated with externalizing phenotypes, including ADHD and cocaine use disorder (CUD). Here, we investigated whether SYT1-rs2251214 could also be implicated with cognitive performance variations among women with CUD. Results showed that G homozygous (n = 146) have lower cognitive performance in the Stroop, Trail Making and Matrix Reasoning tests compared with A-allele carriers (n = 64), suggesting that rs2251214 may influence the severity of cognitive impairments in CUD.
Published: 2019

35. An animal model of what? The case of spontaneously hypertensive rats

Author: Claiton H.D. Bau, Eugenio H. Grevet, Alana Castro Panzenhagen, and Diego L. Rovaris
Subjects: Pharmacology, business.industry, Physiology, Blood Pressure, Rats, Inbred WKY, Rats, Disease Models, Animal, Animal model, Rats, Inbred SHR, Schizophrenia, Medicine, Animals, business, Biological Psychiatry
Published: 2019

36. Shared genetic background between children and adults with attention deficit/hyperactivity disorder

Author: Elizabeth S. Noblin, Joanna L. Mountain, Michelle Agee, Sarah L. Elson, Angélica Salatino-Oliveira, Barbara Franke, Diego L. Rovaris, Josep Antoni Ramos-Quiroga, Vladimir Vacic, Tatyana Strekalova, Claiton H.D. Bau, Christian Fadeuilhe, Peter Almos, Mara H. Hutz, David A. Hinds, Henrik Larsson, Jonna Kuntsi, Olga Rivero, Anders D. Børglum, Laura Vilar, Lorena Arribas, Catherine H. Wilson, Marieke Klein, Adam Auton, Anke Hinney, Katarzyna Bryc, Mark A. Bellgrove, Christie L. Burton, J. Fah Sathirapongsasuti, Olga V. Sazonova, Luis Augusto Rohde, Edmund J.S. Sonuga-Barke, Andreas Reif, Ted Reichborn-Kjennerud, Sarah Kittel-Schneider, Anne Halmøy, Bru Cormand, Miquel Casas, Joyce Y. Tung, Robert D. Oades, Matthew H. McIntyre, Nicholas A. Furlotte, Janie F. Shelton, Alysa E. Doyle, Iris Garcia-Martínez, Marta Ribasés, Johannes Hebebrand, Søren Dalsgaard, Tetyana Zayats, María Soler Artigas, Carrie A.M. Northover, Steven J. Pitts, Ole A. Andreassen, Chao Tian, Karen E. Huber, Josephine Elia, Montserrat Corrales, Jennifer C. McCreight, Benjamin M. Neale, Aribert Rothenberger, Sandra K. Loo, Cristina Sánchez-Mora, Stefan Johansson, Hakon Hakonarson, Christian Jacob, Mireia Pagerols, Jan Haavik, Joseph Biederman, Paula Rovira, Rosa Bosch, Alejandro Arias-Vasquez, Stephen V. Faraone, Catharina A. Hartman, Vanesa Richarte, Oliver Grimm, Irwin D. Waldman, Heike Weber, Martine Hoogman, Per M. Knappskog, Aaron Kleinman, Suyash Shringarpure, Jan K. Buitelaar, Philip Asherson, James J. McGough, Emma Sprooten, Russell Schachar, Ditte Demontis, Klaus-Peter Lesch, Nadia K. Litterman, Gemma Martín, Xin Wang, Evgeniy Svirin, Babak Alipanahi, Ziarih Hawi, Tobias Banaschewski, Bruna Santos da Silva, Robert K. Bell, Eugenio H. Grevet, Pierre Fontanillas, Nina Roth Mota, Jennifer Crosbie, Astri J. Lundervold, Psychiatrie & Neuropsychologie, and RS: MHeNs - R3 - Neuroscience
Subjects: Persistence (psychology), Trastorns per dèficit d'atenció amb hiperactivitat en els infants, SYMPTOMS, LD SCORE REGRESSION, Stress-related disorders Donders Center for Medical Neuroscience [Radboudumc 13], CHILDHOOD, Genome-wide association study, Attention deficit disorder with hyperactivity in children, CA2+-DEPENDENT ACTIVATOR PROTEIN, 0302 clinical medicine, Neurodevelopmental disorder, Child, SECRETION 2, 0303 health sciences, HERITABILITY, 220 Statistical Imaging Neuroscience, Psychiatry and Mental health, Phenotype, Trastorns per dèficit d'atenció amb hiperactivitat en els adults, medicine.symptom, Genetic Background, Clinical psychology, Adult, DEFICIT HYPERACTIVITY DISORDER, Impulsivity, behavioral disciplines and activities, Genetic correlation, Article, 03 medical and health sciences, mental disorders, medicine, Humans, ADHD, Attention deficit hyperactivity disorder, GENOME-WIDE ASSOCIATION, METAANALYSIS, 030304 developmental biology, Genetic association, Pharmacology, Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], business.industry, medicine.disease, Genetic architecture, Attention Deficit Disorder with Hyperactivity, Impulsive Behavior, Attention deficit, Genetic markers, Attention deficit disorder with hyperactivity in adults, business, 030217 neurology & neurosurgery, Genome-Wide Association Study
Abstract: Altres ajuts: VR has served on the speakers for Eli Lilly, Rubio, and Shire in the last 5 years. She has received travel awards from Eli Lilly and Co. and Shire for participating in psychiatric meetings. The ADHD Program has received unrestricted educational and research support from Eli Lilly and Co., Janssen-Cilag, Shire, Rovi, Psious, and Laboratorios Rubió in the past 2 years. MC received travel awards for taking part in psychiatric meetings from Shire. CF received travel awards for taking part in psychiatric meetings from Shire and Lundbeck. GEM received travel awards for taking part in psychiatric meetings from Shire. EJSS-B received speaker fees, consultancy, research funding, and conference support from Shire Pharma. Consultancy from Neurotech Solutions, Copenhagen University and Berhanderling, Skolerne & KU Leuven. Book royalties from OUP and Jessica Kingsley. Financial support-Arhus University and Ghent University for visiting Professorship. Editor-in-Chief JCPP-supported by a buy-out of time to University of Southampton and personal Honorarium. King's College London received payments for work conducted by PA: consultancy for Shire, Eli Lilly, Novartis, and Lundbeck; educational and/or research awards from Shire, Eli Lilly, Novartis, Vifor Pharma, GW Pharma, and QbTech; speaker at events sponsored by Shire, Eli Lilly, Janssen-Cilag, and Novartis. JKB has been in the past 3 years a consultant to/member of advisory board of and/or speaker for Shire, Roche, Medice, and Servier. He is not an employee of any of these companies, and not a stock shareholder of any of these companies. He has no other financial or material support, including expert testimony, patents, royalties. In the past year, SVF received income, potential income, travel expenses continuing education support and/or research support from Tris, Otsuka, Arbor, Ironshore, Shire, Akili Interactive Labs, Enzymotec, Sunovion, Supernus, and Genomind. With his institution, he has US patent US20130217707 A1 for the use of sodium-hydrogen exchange inhibitors in the treatment of ADHD. He also receives royalties from books published by Guilford Press: Straight Talk about Your Child's Mental Health, Oxford University Press: Schizophrenia: The Facts and Elsevier: ADHD: Non-Pharmacologic Interventions. He is principal investigator of www.adhdinadults.com. JK has given talks at educational events sponsored by Medice; all funds are received by King's College London and used for studies of ADHD. HL has served as a speaker for Evolan Pharma and Shire and has received research grants from Shire; all outside the submitted work. K-PL served as a speaker for Eli Lilly and received research support from Medice, and travel support from Shire, all outside the submitted work. LAR reported receiving honoraria, serving on the speakers' bureau/advisory board, and/or acting as a consultant for Eli Lilly, Janssen-Cilag, Novartis, and Shire in the last 3 years; receiving authorship royalties from Oxford Press and ArtMed; and receiving travel awards from Shire for his participation in the 2015 WFADHD meetings and from Novartis to take part of the 2016 AACAP meeting. The ADHD and juvenile bipolar disorder outpatient programs chaired by him received unrestricted educational and research support from the following pharmaceutical companies in the last 3 years: Janssen-Cilag, Novartis, and Shire. MC has received travel grants and research support from Eli Lilly and Co., Janssen-Cilag, Shire, and Lundbeck and served as consultant for Eli Lilly and Co., Janssen-Cilag, Shire, and Lundbeck. BF has received educational speaking fees from Medice and Shire. JAR-Q was on the speakers' bureau and/or acted as consultant for Eli Lilly, Janssen-Cilag, Novartis, Shire, Lundbeck, Almirall, Braingaze, Sincrolab, Medice, and Rubió in the last 5 years. He also received travel awards (air tickets + hotel) for taking part in psychiatric meetings from Janssen-Cilag, Rubió, Shire, Medice, and Eli- Lilly. The Department of Psychiatry chaired by him received unrestricted educational and research support from the following companies in the last 5 years: Eli Lilly, Lundbeck, Janssen- Cilag, Actelion, Shire, Ferrer, Oryzon, Roche, Psious, and Rubió. The other authors have nothing to disclose. All members of the 23andMe Research Team are current or former employees of 23andMe, Inc. and hold stock or stock options in 23andMe. Authors of the ADHD Working group of the PGC that participated in this study: Catharina A. Hartman, Ziarih Hawi, Jennifer Crosbie, Sandra Loo, Josephine Elia, Russell Schachar, Christie Burton, Ted Reichborn-Kjennerud, Aribert Rothenberger, Søren Dalsgaard, Irwin Waldman, Mark Bellgrove, Hakon Hakonarson, Johannes Hebebrand, Anke Hinney, and Robert Oades have nothing to disclose. Joseph Biederman 2019-2020: he received research support from Genentech, Headspace Inc., Lundbeck AS, Neurocentria Inc, Pfizer Pharmaceuticals, Roche TCRC Inc., Shire Pharmaceuticals Inc., Sunovion Pharmaceuticals Inc., and Tris. He was a consultant for Akili, Avekshan, Jazz Pharma, and Shire/Takeda. Through MGH CTNI, he participated in a scientific advisory board for Supernus. Dr Biederman's program has received departmental royalties from a copyrighted rating scale used for ADHD diagnoses, paid by Bracket Global, Ingenix, Prophase, Shire, Sunovion, and Theravance; these royalties were paid to the Department of Psychiatry at MGH. Tobias Banaschewski served in an advisory or consultancy role for Lundbeck, Medice, Neurim Pharmaceuticals, Oberberg GmbH, Shire, and Infectopharm. He received conference support or speaker's fee by Lilly, Medice, and Shire. He received royalties from Hogrefe, Kohlhammer, CIP Medien, and Oxford University Press. James McGough is an expert testimony for Eli Lilly; DSMB for Sunovion. Benjamin Neale is a member of the scientific advisory board at Deep Genomics and consultant for Camp4 Therapeutics, Takeda Pharmaceutical, and Biogen. Ole Andreas Andreassen received speaker's honorarium from Lundbeck, and is a consultant for HealthLytix. The research leading to these results has received funding from the European Community's Seventh Framework Programme (FP7/2007-2013) under grant agreement n° 602805 (Aggressotype) as well as from the European Union H2020 Programme (H2020/2014-2020). The work was also supported by the ECNP Network "ADHD across the Lifespan" (https://www.ecnp.eu/research-innovation/ECNP-networks/List-ECNP-Networks/ADHD.aspx). Over the course of this investigation, PR is a recipient of a pre-doctoral fellowship from the Agència de Gestió d'Ajuts Universitaris i de Recerca (AGAUR), Generalitat de Catalunya, Spain. The iPSYCH project is funded by the Lundbeck Foundation (grant nos. R102-A9118 and R155-2014-1724) and the universities, and university hospitals of Aarhus and Copenhagen. ADB and NRM's work is also supported by the EU's Horizon 2020 programme. Data handling and analysis was supported by NIMH (1U01MH109514-01 to Michael O'Donovan and ADB). CSM is a recipient of a Sara Borrell contract from the Instituto de Salud Carlos III, Ministerio de Economía, Industria y Competitividad, Spain. K-PL and his team are supported by the Deutsche Forschungsgemeinschaft (DFG: CRU 125, CRC TRR 58 A1/A5, no. 44541416), ERA-Net NEURON/RESPOND, no. 01EW1602B, ERA-Net NEURON/DECODE, no. 01EW1902, and 5-100 Russian Academic Excellence Project. JH thanks Stiftelsen K.G. Jebsen, University of Bergen, the Western Norwegian Health Authorities (Helse Vest). HL thanks the Swedish research council. BC received financial support from the Spanish "Ministerio de Economía y Competitividad" and AGAUR. MSA is a recipient of a contract from the Biomedical Network Research Center on Mental Health (CIBERSAM), Madrid, Spain. MR is a recipient of a Miguel de Servet contract from the Instituto de Salud Carlos III, Spain. The research leading to these results has received funding from the Instituto de Salud Carlos III , and cofinanced by the European Regional Development Fund (ERDF), from the Pla estratègic de recerca i innovació en salut (PERIS); Generalitat de Catalunya, from "la Marató de TV3" (092330/31) and from the Agència de Gestió d'Ajuts Universitaris i de Recerca-AGAUR, Generalitat de Catalunya. ES's work is supported by a personal Hypatia grant from the Radboud University Medical Center. MH received a Veni grant from of the Netherlands Organization for Scientific Research (NWO, grant number 91619115). The NeuroIMAGE study was supported by NIH Grant R01MH62873 (to SVF), NWO Large Investment Grant 1750102007010 (to JKB), ZonMW grant 60-60600-97-193, NWO grants 056-13-015 and 433-09-242, and matching grants from Radboud University Nijmegen Medical Center, University Medical Center Groningen and Accare, and Vrije Universiteit Amsterdam. Organization for Scientific Research (NWO; grant 016-130-669). BF and MK's work is supported by the Dutch National Science Agenda (NWA) for the NeurolabNL project (grant 400-17-602). This paper represents independent research part funded by the National Institute for Health Research (NIHR) Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London. BF received additional funding from a personal Vici grant of the Dutch. Attention deficit/hyperactivity disorder (ADHD) is a common neurodevelopmental disorder characterized by age-inappropriate symptoms of inattention, impulsivity, and hyperactivity that persist into adulthood in the majority of the diagnosed children. Despite several risk factors during childhood predicting the persistence of ADHD symptoms into adulthood, the genetic architecture underlying the trajectory of ADHD over time is still unclear. We set out to study the contribution of common genetic variants to the risk for ADHD across the lifespan by conducting meta-analyses of genome-wide association studies on persistent ADHD in adults and ADHD in childhood separately and jointly, and by comparing the genetic background between them in a total sample of 17,149 cases and 32,411 controls. Our results show nine new independent loci and support a shared contribution of common genetic variants to ADHD in children and adults. No subgroup heterogeneity was observed among children, while this group consists of future remitting and persistent individuals. We report similar patterns of genetic correlation of ADHD with other ADHD-related datasets and different traits and disorders among adults, children, and when combining both groups. These findings confirm that persistent ADHD in adults is a neurodevelopmental disorder and extend the existing hypothesis of a shared genetic architecture underlying ADHD and different traits to a lifespan perspective.
Published: 2019
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37. The association between SYT1-rs2251214 and cocaine use disorder further supports its role in psychiatry

Author: Eugenio H. Grevet, Cibele Edom Bandeira, Rodrigo Grassi-Oliveira, Renata B. Cupertino, Bruna Santos da Silva, Djenifer B. Kappel, Felix Kessler, Jaqueline Bohrer Schuch, Breno Sanvicente-Vieira, Diego L. Rovaris, Lisia von Diemen, and Claiton H.D. Bau
Subjects: Adult, Male, medicine.medical_specialty, Candidate gene, media_common.quotation_subject, Context (language use), Polymorphism, Single Nucleotide, 03 medical and health sciences, Cocaine-Related Disorders, Young Adult, 0302 clinical medicine, Genetic model, Medicine, Humans, Genetic Predisposition to Disease, Allele, Psychiatry, Biological Psychiatry, Genetic Association Studies, media_common, Pharmacology, business.industry, Methylphenidate, Addiction, Antisocial personality disorder, medicine.disease, 030227 psychiatry, Synaptic vesicle exocytosis, Case-Control Studies, Synaptotagmin I, Crack Cocaine, Female, business, medicine.drug
Abstract: Synaptotagmin-1 is an essential regulator of synaptic vesicle exocytosis, and its encoding gene (SYT1) is a genome and transcriptome-wide association hit in cognitive performance, personality and cocaine use disorder (CUD) studies. Additionally, in candidate gene studies the specific variant rs2251214 has been associated with attention-deficit/hyperactivity disorder (ADHD), antisocial personality disorder and other externalizing phenotypes in adults with ADHD, as well as with response to methylphenidate (MPH) treatment. In this context, we sought to evaluate, in an independent sample, the association of this variant with CUD, a phenotype that shares common biological underpinnings with the previously associated traits. We tested the association between SYT1-rs2251214 and CUD susceptibility and severity (addiction severity index) in a sample composed by 315 patients addicted to smoked cocaine and 769 non-addicted volunteers. SYT1-rs2251214 was significantly associated with susceptibility to CUD, where the G allele presented increased risk for the disorder in the genetic models tested (P = 0.0021, OR = 1.44, allelic; P = 0.0012, OR = 1.48, additive; P = 0.0127, OR = 1.41, dominant). This is the same allele that was associated with increased risk for ADHD and other externalizing behaviors, as well as poor response to MPH treatment in previous studies. These findings suggest that the neurotransmitter exocytosis pathway might play a critical role in the liability for psychiatric disorders, especially externalizing behaviors and CUD.
Published: 2019

38. Integrative proteomics and pharmacogenomics analysis of methylphenidate treatment response

Author: Douglas Teixeira Leffa, Markus Berger, Claiton H.D. Bau, Ramon Diaz Pena, Iraci Lucena da Silva Torres, Eugenio H. Grevet, John R. Yates, Bruna Santos da Silva, Carla de Oliveira, Renuka Sabnis, Verônica Contini, Marcelo M. Victor, Alexandre Rosa Campos, Walter O. Beys-da-Silva, Diego L. Rovaris, Lucélia Santi, Luis Augusto Rohde, and Nina Roth Mota
Subjects: Adult, Male, Proteomics, Candidate gene, Pharmacology, Biology, Rats, Inbred WKY, Article, lcsh:RC321-571, Biological pathway, Random Allocation, 03 medical and health sciences, Cellular and Molecular Neuroscience, chemistry.chemical_compound, 0302 clinical medicine, All institutes and research themes of the Radboud University Medical Center, mental disorders, medicine, ADHD, Animals, Humans, Neurotransmitter, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Biological Psychiatry, 030304 developmental biology, 0303 health sciences, Proteômica, Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], Proteomic Profiling, Methylphenidate, Transtorno do déficit de atenção com hiperatividade, Rats, 3. Good health, Psychiatry and Mental health, chemistry, Attention Deficit Disorder with Hyperactivity, Pharmacogenetics, Pharmacogenomics, Central Nervous System Stimulants, Female, human activities, Metilfenidato, 030217 neurology & neurosurgery, medicine.drug
Abstract: Transcriptomics and candidate gene/protein expression studies have indicated several biological processes modulated by methylphenidate (MPH), widely used in attention-deficit/hyperactivity disorder (ADHD) treatment. However, the lack of a differential proteomic profiling of MPH treatment limits the understanding of the most relevant mechanisms by which MPH exerts its pharmacological effects at the molecular level. Therefore, our aim is to investigate the MPH-induced proteomic alterations using an experimental design integrated with a pharmacogenomic analysis in a translational perspective. Proteomic analysis was performed using the cortices of Wistar-Kyoto rats, which were treated by gavage with MPH (2 mg/kg) or saline for two weeks (n = 6/group). After functional enrichment analysis of the differentially expressed proteins (DEP) in rats, the significant biological pathways were tested for association with MPH response in adults with ADHD (n = 189) using genome-wide data. Following MPH treatment in rats, 98 DEPs were found (P 1.0). The functional enrichment analysis of the DEPs revealed 18 significant biological pathways (gene-sets) modulated by MPH, including some with recognized biological plausibility, such as those related to synaptic transmission. The pharmacogenomic analysis in the clinical sample evaluating these pathways revealed nominal associations for gene-sets related to neurotransmitter release and GABA transmission. Our results, which integrate proteomics and pharmacogenomics, revealed putative molecular effects of MPH on several biological processes, including oxidative stress, cellular respiration, and metabolism, and extended the results involving synaptic transmission pathways to a clinical sample. These findings shed light on the molecular signatures of MPH effects and possible biological sources of treatment response variability.
Published: 2019

39. Childhood Physical Neglect is Associated With Epigenetic Aging Acceleration Among Women With Cocaine Use Disorder

Author: Diego L. Rovaris, Rodrigo Grassi-Oliveira, Thiago Wendt Viola, Eugeunio Grevet, Consuelo Walss Bass, Joy M. Schmitz, Gabriel Rodrigo Fries, and Claiton H.D. Bau
Subjects: business.industry, Cocaine use, Medicine, Acceleration (differential geometry), Epigenetics, business, Biological Psychiatry, Physical neglect, Developmental psychology
Published: 2021
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40. Exploring DSM-5 ADHD criteria beyond young adulthood: phenomenology, psychometric properties and prevalence in a large three-decade birth cohort

Author: Christian Kieling, Fernando C. Barros, Giovanni Abrahão Salum, Bernardo L. Horta, Luiz Rohde, R T Pinheiro, Claiton H.D. Bau, Eugenio H. Grevet, Eduardo S. Vitola, and Luciana de Avila Quevedo
Subjects: Adult, Male, medicine.medical_specialty, Psychometrics, Population, Prevalence, Sensitivity and Specificity, behavioral disciplines and activities, DSM-5, Cohort Studies, 03 medical and health sciences, 0302 clinical medicine, mental disorders, medicine, Humans, Attention deficit hyperactivity disorder, Young adult, education, Psychiatry, Applied Psychology, Psychometry, Psychiatric Status Rating Scales, education.field_of_study, Receiver operating characteristic, business.industry, Discriminant validity, Reproducibility of Results, medicine.disease, 030227 psychiatry, Diagnostic and Statistical Manual of Mental Disorders, Psychiatry and Mental health, Cross-Sectional Studies, Attention Deficit Disorder with Hyperactivity, Female, business, Brazil, 030217 neurology & neurosurgery
Abstract: BackgroundThere are still uncertainties on the psychometric validity of the DSM-5 attention deficit hyperactivity disorder (ADHD) criteria for its use in the adult population. We aim to describe the adult ADHD phenotype, to test the psychometric properties of the DSM-5 ADHD criteria, and to calculate the resulting prevalence in a population-based sample in their thirties.MethodA cross-sectional evaluation using the DSM-5 ADHD criteria was carried out in 3574 individuals from the 1982 Pelotas Birth Cohort. Through receiver operator curve, latent and regression analyses, we obtained parameters on construct and discriminant validity. Still, prevalence rates were calculated for different sets of criteria.ResultsThe latent analysis suggested that the adult ADHD phenotype is constituted mainly by inattentive symptoms. Also, inattention symptoms were the symptoms most associated with impairment. The best cut-off for diagnosis was four symptoms, but sensitivity and specificity for this cut-off was low. ADHD prevalence rates were 2.1% for DSM-5 ADHD criteria and 5.8% for ADHD disregarding age-of-onset criterion.ConclusionsThe bi-dimensional ADHD structure proposed by the DSM demonstrated both construct and discriminant validity problems when used in the adult population, since inattention is a much more relevant feature in the adult phenotype. The use of the DSM-5 criteria results in a higher prevalence of ADHD when compared to those obtained by DSM-IV, and prevalence would increase almost threefold when considering current ADHD syndrome. These findings suggest a need for further refinement of the criteria for its use in the adult population.
Published: 2016
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41. Pleiotropic effects of Chr15q25 nicotinic gene cluster and the relationship between smoking, cognition and ADHD

Author: Djenifer B. Kappel, Rafael G. Karam, Nina Roth Mota, Eugenio H. Grevet, Evelise R. Polina, Luis Augusto Rohde, Jaqueline Bohrer Schuch, Melanie J. White, Renata B. Cupertino, Claiton H.D. Bau, Paula O. Guimarães-da-Silva, Katiane L. Silva, Carlos A.I. Salgado, and Diego L. Rovaris
Subjects: Adult, Male, 0301 basic medicine, Genotype, Neuropsychological Tests, Receptors, Nicotinic, Polymorphism, Single Nucleotide, Linkage Disequilibrium, Developmental psychology, Nicotine, 03 medical and health sciences, 0302 clinical medicine, mental disorders, Gene cluster, medicine, Humans, Genetic Predisposition to Disease, Effects of sleep deprivation on cognitive performance, Biological Psychiatry, Psychiatric Status Rating Scales, Analysis of Variance, Chromosomes, Human, Pair 15, biology, CHRNA5, Neuropsychology, Wechsler Adult Intelligence Scale, Cognition, Tobacco Use Disorder, Middle Aged, Psychiatry and Mental health, 030104 developmental biology, Nicotinic agonist, Attention Deficit Disorder with Hyperactivity, Multigene Family, biology.protein, Female, Cognition Disorders, Psychology, 030217 neurology & neurosurgery, medicine.drug
Abstract: Polymorphisms in the CHRNA5-CHRNA3-CHRNB4 gene cluster (Chr15q25) have been robustly associated with nicotine dependence, including genome-wide studies, as well as with cognitive and neuropsychological measures. In addition, cognitive processes can be influenced by nicotine use through nicotinic acetylcholine receptors (nAChRs). Here, we evaluated the effect of polymorphisms in CHRNA5-CHRNA3-CHRNB4 gene cluster and their interaction with tobacco smoking status on cognition in patients with Attention Deficit/Hyperactivity Disorder (ADHD). Eight SNPs from the CHRNA5-CHRNA3-CHRNB4 gene cluster were evaluated on a clinical sample of 403 adults with ADHD. Cognitive performance was assessed using the Wechsler Adult Intelligence Scale-Revised (WAIS-R). Analyses of covariance were used to assess the influence of single markers and their interaction with smoking status in the Vocabulary and Block Design subtests of WAIS-R. Correction for multiple comparisons was applied. Lifetime smoking was associated to Vocabulary subtest. The TT genotypes of CHRNA5 SNPs rs588765 and rs514743 showed a trend towards association with, respectively, higher and lower scores on the Vocabulary subtest. There was a significant interaction between intergenic SNP rs8023462 and smoking on Vocabulary scores. Our results are consistent with an influence of variants in the CHRNA5-CHRNA3-CHRNB4 gene cluster on cognitive measures. The overall scenario suggests a pleiotropic role of Chr15q25 nicotinic gene cluster with complex influences in ADHD, tobacco smoking and cognitive performance, characteristics that can be partially interdependent and may share underlying genetic factors.
Published: 2016
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42. Glucocorticoid receptor gene modulates severity of depression in women with crack cocaine addiction

Author: Djenifer B. Kappel, Adriana Raquel Binsfeld Hess, Diego L. Rovaris, Bruna Santos da Silva, Rosa Maria Martins de Almeida, Rodrigo Grassi-Oliveira, Jaqueline Bohrer Schuch, Mateus Luz Levandowski, Julio Carlos Pezzi, Angelita P. Aroche, and Claiton H.D. Bau
Subjects: Adult, medicine.medical_specialty, Genotyping Techniques, media_common.quotation_subject, Physiology, Single-nucleotide polymorphism, Polymorphism, Single Nucleotide, Receptors, Corticotropin-Releasing Hormone, Tacrolimus Binding Proteins, Cocaine-Related Disorders, Young Adult, 03 medical and health sciences, Receptors, Glucocorticoid, 0302 clinical medicine, medicine, Humans, Pharmacology (medical), Longitudinal Studies, Allele, Psychiatry, Biological Psychiatry, Depression (differential diagnoses), media_common, Pharmacology, Depression, Genetic heterogeneity, Abstinence, medicine.disease, Substance Withdrawal Syndrome, 030227 psychiatry, Hospitalization, Minor allele frequency, Psychiatry and Mental health, Receptors, Mineralocorticoid, Neurology, Crack Cocaine, Regression Analysis, Major depressive disorder, Female, Neurology (clinical), FKBP5, Psychology, 030217 neurology & neurosurgery, Follow-Up Studies
Abstract: Crack cocaine addicted inpatients that present more severe withdrawal symptoms also exhibit higher rates of depressive symptoms. There is strong evidence that the identification of genetic variants in depression is potentialized when reducing phenotypic heterogeneity by studying selected groups. Since depression has been associated to dysregulation of the hypothalamic-pituitary-adrenal axis, this study evaluated the effects of SNPs in stress-related genes on depressive symptoms of crack cocaine addicts at early abstinence and over the detoxification treatment (4th, 11th and 18th day post admission). Also, the role of these SNPs on the re-hospitalization rates after 2.5 years of follow-up was studied. One hundred eight-two women were enrolled and eight SNPs in four genes (NR3C2, NR3C1, FKBP5 and CRHR1) were genotyped. A significant main effect of NR3C1-rs41423247 was found, where the C minor allele increased depressive symptoms at early abstinence. This effect remained significant after 10,000 permutations to account for multiple SNPs tested (P=0.0077). There was no effect of rs41423247 on the course of detoxification treatment, but a slight effect of rs41423247 at late abstinence was detected (P=0.0463). This analysis suggests that the presence of at least one C allele is worse at early abstinence, while only CC genotype appears to increase depressive symptoms at late abstinence. Also, a slight effect of rs41423247 C minor allele increasing the number of re-hospitalizations after 2.5 years was found (P=0.0413). These findings are in agreement with previous studies reporting an influence of rs41423247 on sensitivity to glucocorticoids and further elucidate its resulting effects on depressive-related traits.
Published: 2016
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43. Predictors of persistence of ADHD into adulthood: a systematic review of the literature and meta-analysis

Author: Rafael G. Karam, Eugenio H. Grevet, Alex Vicente Spadini, Christian Kieling, Claiton H.D. Bau, Luis Augusto Rohde, Diego L. Rovaris, and Arthur Caye
Subjects: Adult, medicine.medical_specialty, Adolescent, Population, Comorbidity, 03 medical and health sciences, 0302 clinical medicine, Neurodevelopmental disorder, Developmental and Educational Psychology, medicine, Child and adolescent psychiatry, Humans, Child, education, education.field_of_study, General Medicine, medicine.disease, 030227 psychiatry, Psychiatry and Mental health, Attention Deficit Disorder with Hyperactivity, Conduct disorder, Meta-analysis, Pediatrics, Perinatology and Child Health, Major depressive disorder, Psychology, 030217 neurology & neurosurgery, Cohort study, Clinical psychology
Abstract: Attention-deficit/hyperactivity disorder (ADHD) is traditionally conceptualized as a neurodevelopmental disorder that continues into adulthood in up to half of diagnosed cases. In light of current evidence, factors associated with the course of the disorder remain unknown. We performed a systematic review of the literature searching for risk markers from childhood that predicted the persistence of ADHD into adulthood. We reviewed 26,168 abstracts and selected 72 for full-text review. We identified data from 16 studies, comprising 6 population-based retrospective samples and 10 clinical follow-ups. We performed meta-analyses of factors evaluated by at least three studies. Severity of ADHD (OR 2.33, 95 % CI = 1.6–3.39, p < 0.001), treatment for ADHD (OR 2.09, 95 % CI = 1.04–4.18, p = 0.037), comorbid conduct disorder (OR 1.85, 95 % CI = 1.06–3.24, p = 0.030), and comorbid major depressive disorder (OR 1.8, 95 % CI = 1.1–2.95, p = 0.019) emerged as predictors already presented in childhood for ADHD persistence into adulthood. Further, we suggest that cohort studies should be designed to clarify such an important question for research and clinical practice.
Published: 2016
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44. SNARE complex in developmental psychiatry: neurotransmitter exocytosis and beyond

Author: Djenifer B. Kappel, Diana Müller, Nina Roth Mota, Renata B. Cupertino, Cibele Edom Bandeira, Bruna Santos da Silva, Jaqueline Bohrer Schuch, and Claiton H.D. Bau
Subjects: 0301 basic medicine, medicine.medical_specialty, Biology, Exocytosis, Synaptotagmin 1, 03 medical and health sciences, medicine, Humans, Psychiatry, Biological Psychiatry, Neurotransmitter Agents, VAMP2, STX1A, Mental Disorders, SNAP25, Transport protein, Protein Transport, Psychiatry and Mental health, 030104 developmental biology, Neurology, Membrane protein, Pharmacogenetics, Neurology (clinical), SNARE Proteins, SNARE complex, Protein Processing, Post-Translational, Neuroscience
Abstract: Multiple biological processes throughout development require intracellular vesicular trafficking, where the SNARE (soluble N-ethylmaleimide-sensitive factor (NSF) attachment protein (SNAP) receptors) complex plays a major role. The core proteins forming the SNARE complex are SNAP-25 (synaptosomal-associated protein 25), VAMP (vesicle-associated membrane protein) and Syntaxins, besides its regulatory proteins, such as Synaptotagmin. Genes encoding these proteins (SNAP25, VAMP1, VAMP2, STX1A, SYT1 and SYT2) have been studied in relation to psychiatric disorders susceptibility. Here, we review physiological aspects of SNARE complex and genetic association results reported for attention deficit hyperactivity disorder, both in children and adults, autism spectrum disorders, major depressive disorder, bipolar disorder and schizophrenia. Moreover, we included findings from expression, pharmacogenetics and animal model studies regarding these clinical phenotypes. The overall scenario depicted here suggests that the SNARE complex may exert distinct roles throughout development, with age-specific effects of genetic variants in psychiatric disorders. Such perspective should be considered in future studies regarding SNARE complex genes.
Published: 2016
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45. Methylphenidate Alters Functional Connectivity of Default Mode Network in Drug-Naive Male Adults With ADHD

Author: Bruna Bressan Valentini, Alessandro André Mazzola, Neivo da Silva, Eugenio H. Grevet, Marcelo M. Victor, João Ricardo Sato, Vitor Breda, Rafael G. Karam, Felipe Almeida Picon, Luis Augusto Rohde, Katiane L. Silva, Leonardo Modesti Vedolin, Maurício Anés, Renata B. Cupertino, and Claiton H.D. Bau
Subjects: Adult, Male, Posterior parietal cortex, Gyrus Cinguli, 03 medical and health sciences, 0302 clinical medicine, Neurodevelopmental disorder, Cortex (anatomy), mental disorders, Developmental and Educational Psychology, medicine, Humans, 0501 psychology and cognitive sciences, Default mode network, Brain Mapping, medicine.diagnostic_test, Methylphenidate, 05 social sciences, Brain, medicine.disease, Magnetic Resonance Imaging, Clinical Psychology, Drug-naïve, medicine.anatomical_structure, Attention Deficit Disorder with Hyperactivity, Posterior cingulate, Functional magnetic resonance imaging, Psychology, human activities, Neuroscience, 030217 neurology & neurosurgery, 050104 developmental & child psychology, medicine.drug
Abstract: Objective: This study evaluated the hypothesis that methylphenidate immediate release (MPH-IR) treatment would improve Default Mode Network (DMN) within-connectivity. Method: Resting-state functional connectivity of the main nodes of DMN was evaluated in a highly homogeneous sample of 18 drug-naive male adult participants with ADHD. Results: Comparing resting-state functional connectivity functional magnetic resonance imaging (R-fMRI) scans before and after MPH treatment focusing exclusively on within-DMN connectivity, we evidenced the strengthening of functional connectivity between two nodes of the DMN: posterior cingulate cortex (PCC) and left lateral parietal cortex (LLP). Conclusion: Our results contribute to the further understanding on how MPH affects functional connectivity within DMN of male adults with ADHD and corroborate the hypothesis of ADHD being a delayed neurodevelopmental disorder.
Published: 2018

46. Behavioural effects of methylphenidate in the spontaneously hypertensive rat model of attention-deficit/hyperactivity disorder: a systematic review and meta-analysis protocol

Author: Diego L. Rovaris, Eugenio H. Grevet, Douglas Teixeira Leffa, Luis Augusto Rohde, Claiton H.D. Bau, Gabriel Natan Pires, and Alana Castro Panzenhagen
Subjects: 0301 basic medicine, Predictive validity, MEDLINE, lcsh:Medicine, methylphenidate, Impulsivity, 03 medical and health sciences, 0302 clinical medicine, Protocol, medicine, Attention deficit hyperactivity disorder, Protocol (science), business.industry, Methylphenidate, lcsh:R, attention deficit disorder with hyperactivity, General Medicine, medicine.disease, meta-analysis as topic, rats, inbred SHR, 030104 developmental biology, Data extraction, Meta-analysis, medicine.symptom, business, 030217 neurology & neurosurgery, Clinical psychology, medicine.drug
Abstract: Introduction Attention-deficit/hyperactivity disorder (ADHD) is a prevalent condition related to several negative outcomes, and its pathophysiology is still poorly understood. The spontaneously hypertensive rats (SHRs) are the most commonly used animal model of ADHD. How ever, its validity, and especially its predictive validity, has been questioned. Therefore, the current protocol discloses the background, aims and methods of a systematic review and meta-analysis of studies reporting the behavioural effects of methylphenidate (MPH), the most commonly prescribed treatment for ADHD, in the SHR. Search strategy Studies will be identified through a literature search using three different electronic databases: Medline, Embase and Web of Science. There will be no language restrictions. All s tudies that administered MPH to SHR and evaluated locomotion, attention, impulsivity or memory will be included. Screening and annotation Studies will be prescreened based on title and abstract, and a full-text review will be performed if necessary. Screening will be performed by two authors, and any disagreement will be discussed with a third author. Data management and reporting Data extraction will be performed by two independent authors according to a standardised form. Studies will be grouped according to the behavioural outcomes reported, and a meta-analysis will be performed for each group. The influence of predefined covariates on the effects of MPH will be evaluated using meta-regression and sensitivity analyses. Data will be reported following PRISMA guidelines.
Published: 2018
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47. Increase of global DNA methylation patterns in beauty salon workers exposed to low levels of formaldehyde

Author: Diana Müller, Diego L. Rovaris, Ana Laura Anibaletto dos Santos, Mariele Feiffer Charão, Rafael Linden, Eduardo Barbosa, Claiton H.D. Bau, Giovana Piva Peteffi, Anelise Schneider, and Marina Venzon Antunes
Subjects: Health, Toxicology and Mutagenesis, Formaldehyde, Air Pollutants, Occupational, 010501 environmental sciences, 01 natural sciences, Group A, Group B, Andrology, chemistry.chemical_compound, Beauty, Occupational Exposure, Environmental Chemistry, Medicine, Humans, Epigenetics, Hair straightening, Carcinogen, 0105 earth and related environmental sciences, business.industry, General Medicine, DNA Methylation, Pollution, chemistry, DNA methylation, Occupational exposure, business, Brazil
Abstract: Formaldehyde (FA) is a carcinogenic aldehyde illegally added to creams as a hair straightening agent for the Brazilian blowout (BB). This study aimed to investigate the possible effects of occupational exposure to FA on global DNA methylation in salon workers with different exposure levels. FA exposure was monitored using environmental and biological measurements. The study included 49 salon workers divided by FA levels in the workplace into group A (FA
Published: 2018

48. ADGRL3 rs6551665 as a Common Vulnerability Factor Underlying Attention-Deficit/Hyperactivity Disorder and Autism Spectrum Disorder

Author: Djenifer B. Kappel, Vitor Breda, Stefania Pigatto Teche, Bruna Santos da Silva, Diana Müller, Eugenio H. Grevet, Diego L. Rovaris, Claiton H.D. Bau, Lavinia Schuler-Faccini, Luis Augusto Rohde, Rudimar dos Santos Riesgo, and Jaqueline Bohrer Schuch
Subjects: 0301 basic medicine, Adult, Male, medicine.medical_specialty, Brain development, Neurology, Adolescent, Receptors, Peptide, Autism Spectrum Disorder, Nerve Tissue Proteins, behavioral disciplines and activities, Polymorphism, Single Nucleotide, Vulnerability factor, Receptors, G-Protein-Coupled, 03 medical and health sciences, Cellular and Molecular Neuroscience, Young Adult, 0302 clinical medicine, Age Distribution, mental disorders, medicine, Attention deficit hyperactivity disorder, Humans, Computer Simulation, Genetic Predisposition to Disease, Age of Onset, Sex Distribution, Child, Models, Genetic, business.industry, Brain, Gene Expression Regulation, Developmental, medicine.disease, Comorbidity, 030104 developmental biology, Increased risk, Autism spectrum disorder, Attention Deficit Disorder with Hyperactivity, Neurodevelopmental Disorders, Molecular Medicine, business, 030217 neurology & neurosurgery, Clinical psychology
Abstract: Neurodevelopmental disorders are prevalent, frequently occur in comorbidity and share substantial genetic correlation. Previous evidence has suggested a role for the ADGRL3 gene in Attention-Deficit/Hyperactivity Disorder (ADHD) susceptibility in several samples. Considering ADGRL3 functionality in central nervous system development and its previous association with neurodevelopmental disorders, we aimed to assess ADGRL3 influence in early-onset ADHD (before 7 years of age) and Autism Spectrum Disorder (ASD). The sample comprises 187 men diagnosed with early-onset ADHD, 135 boys diagnosed with ASD and 468 male blood donors. We tested the association of an ADGRL3 variant (rs6551665) with both early-onset ADHD and ASD susceptibility. We observed significant associations between ADGRL3—rs6551665 on ADHD and ASD susceptibilities; we found that G-carriers were at increased risk of ADHD and ASD, in accordance with previous studies. The overall evidence from the literature, corroborated by our results, suggests that ADGRL3 might be involved in brain development, and genetic modifications related to it might be part of a shared vulnerability factor associated with the underlying neurobiology of neurodevelopmental disorders such as ADHD and ASD.
Published: 2018

49. Integrative genomic analysis of methylphenidate response in attention-deficit/hyperactivity disorder

Author: Josep Antoni Ramos-Quiroga, Nina Roth Mota, Iris Garcia-Martínez, Marta Ribasés, Claiton H.D. Bau, Vanesa Richarte, Eugenio H. Grevet, Bruna Santos da Silva, Paula Rovira, Bru Cormand, Marcelo M. Victor, María Soler Artigas, Luis Augusto Rohde, Miguel Casas, Cristina Sánchez-Mora, Montse Corrales, Mireia Pagerols, Eva Calvo-Sánchez, and Universitat de Barcelona
Subjects: Male, 0301 basic medicine, Trastorns per dèficit d'atenció amb hiperactivitat en els infants, lcsh:Medicine, Genome-wide association study, Bioinformatics, Attention deficit disorder with hyperactivity in children, 0302 clinical medicine, Human genetics, Polymorphism (computer science), Child, lcsh:Science, Polimorfismo de nucleotídeo único, Genètica humana, Multidisciplinary, Adulto, Methylphenidate, Genomics, Human brain, Transtorno do déficit de atenção com hiperatividade, Treatment Outcome, medicine.anatomical_structure, Child, Preschool, Cohort, Female, Metilfenidato, medicine.drug, Nervous system, Adolescent, Single-nucleotide polymorphism, Polymorphism, Single Nucleotide, Article, 03 medical and health sciences, All institutes and research themes of the Radboud University Medical Center, mental disorders, medicine, Humans, Attention deficit hyperactivity disorder, Sistema nerviós, Attention-deficit-disordered children, Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], business.industry, lcsh:R, medicine.disease, Trastorns per dèficit d'atenció en els infants, 030104 developmental biology, Attention Deficit Disorder with Hyperactivity, Expression quantitative trait loci, Central Nervous System Stimulants, lcsh:Q, business, 030217 neurology & neurosurgery, Genome-Wide Association Study
Abstract: Methylphenidate (MPH) is the most frequently used pharmacological treatment in children with attention-deficit/hyperactivity disorder (ADHD). However, a considerable interindividual variability exists in clinical outcome. Thus, we performed a genome-wide association study of MPH efficacy in 173 ADHD paediatric patients. Although no variant reached genome-wide significance, the set of genes containing single-nucleotide polymorphisms (SNPs) nominally associated with MPH response (P cis-eQTL in 32 different loci (referred to as eSNPs and eGenes, respectively). Pathway enrichment analyses revealed an over-representation of genes involved in nervous system development and function among the eGenes. Categories related to neurological diseases, psychological disorders and behaviour were also significantly enriched. We subsequently meta-analysed the association with clinical outcome for the 33 eSNPs across the discovery sample and an independent cohort of 189 ADHD adult patients (target sample) and we detected 15 suggestive signals. Following this comprehensive strategy, our results provide a better understanding of the molecular mechanisms implicated in MPH treatment effects and suggest promising candidates that may encourage future studies.
Published: 2018
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50. The impact of the overlap between externalizing and internalizing problems on substance use disorders

Author: Carlos A.I. Salgado, Claiton H.D. Bau, Eduardo S. Vitola, Eugenio H. Grevet, and Diego L. Rovaris
Subjects: Problem Behavior, medicine.medical_specialty, Adolescent, Substance-Related Disorders, General Medicine, Scandinavian and Nordic Countries, Psychiatry and Mental health, Pediatrics, Perinatology and Child Health, Developmental and Educational Psychology, Child and adolescent psychiatry, medicine, Humans, Substance use, Psychology, Psychiatry
Published: 2019
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