Authors

Mauricio Arcos-Burgos, National Human Genome Research Institute
Jorge I. Vélez, National Human Genome Research Institute
Ariel F. Martinez, National Human Genome Research Institute
Marta Ribasés, Universitat Autònoma de Barcelona, Spain
Josep A. Ramos-Quiroga, Universitat Autònoma de Barcelona, Spain
Cristina Sánchez-Mora, Universitat Autònoma de Barcelona, Spain
Vanesa Richarte, Hospital Universitari Vall d’Hebron, Spain
Carlos Roncero, Hospital Universitari Vall d’Hebron, Spain
Bru Cormand, University of Barcelona, Spain
Noelia Fernández-Castillo, University of Barcelona, Spain
Miguel Casas, Universitat Autònoma de Barcelona, Spain
Francisco Lopera, Universidad de Antioquia, Colombia
David A. Pineda, Universidad de Antioquia, Colombia
Juan D. Palacio, Universidad de Antioquia, Colombia
Johan E. Acosta-López, Universidad Simón Bolívar, Colombia
Martha L. Cervantes-Henriquez, Universidad del Norte, Colombia
Manuel G. Sánchez-Rojas, Universidad Simón Bolívar, Colombia
Pedro J. Puentes-Rozo, Universidad Simón Bolívar, Colombia
Brooke S. G. Molina, University of Pittsburgh
MTA Cooperative Group
Margaret T. Boden, University of Kentucky
Deeann Wallis, Texas A & M University
Brett Lidbury, The Australian National University, Australia
Saul Newman, The Australian National University, Australia
Simon Easteal, The Australian National University, Australia
James Swanson, University of California - Irvine
Hardip Patel, The Australian National University, Australia
Nora Volkow, National Institute on Drug Abuse
Maria T. Acosta, National Human Genome Research Institute
Francisco X. Castellanos, New York University
Jose de Leon, University of KentuckyFollow

Abstract

Genetic factors are strongly implicated in the susceptibility to develop externalizing syndromes such as attention-deficit/hyperactivity disorder (ADHD), oppositional defiant disorder, conduct disorder, and substance use disorder (SUD). Variants in the ADGRL3 (LPHN3) gene predispose to ADHD and predict ADHD severity, disruptive behaviors comorbidity, long-term outcome, and response to treatment. In this study, we investigated whether variants within ADGRL3 are associated with SUD, a disorder that is frequently co-morbid with ADHD. Using family-based, case-control, and longitudinal samples from disparate regions of the world (n = 2698), recruited either for clinical, genetic epidemiological or pharmacogenomic studies of ADHD, we assembled recursive-partitioning frameworks (classification tree analyses) with clinical, demographic, and ADGRL3 genetic information to predict SUD susceptibility. Our results indicate that SUD can be efficiently and robustly predicted in ADHD participants. The genetic models used remained highly efficient in predicting SUD in a large sample of individuals with severe SUD from a psychiatric institution that were not ascertained on the basis of ADHD diagnosis, thus identifying ADGRL3 as a risk gene for SUD. Recursive-partitioning analyses revealed that rs4860437 was the predominant predictive variant. This new methodological approach offers novel insights into higher order predictive interactions and offers a unique opportunity for translational application in the clinical assessment of patients at high risk for SUD.

Document Type

Article

Publication Date

1-29-2019

Notes/Citation Information

Published in Translational Psychiatry, v. 9, article no. 42, p. 1-15.

© The Author(s) 2019

This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

Due to the large number of authors, only the first 30 and the authors affiliated with the University of Kentucky are listed in the author section above. For the complete list of authors, please download this article or visit: https://doi.org/10.1038/s41398-019-0396-7

Digital Object Identifier (DOI)

https://doi.org/10.1038/s41398-019-0396-7

Funding Information

This study was supported by the National Human Genome Research Institute intramural funds (to M.M.) for the ascertainment of patients from the Paisa population. The Kentucky sample was ascertained using funds from the Eli Lilly Research Foundation (to J.d.L.), a National Alliance for Research on Schizophrenia and Depression (NARSAD) Independent Award (to J.d.L.), University of Kentucky internal funding (to J.d.L.), and Roche Molecular Systems, Inc., who provided free genotyping and laboratory supplies (to J.d.L.). J.I.V. is partially supported by research grant FOFICO 32101-511035-PE0031 from Universidad del Norte, Barranquilla, Colombia. The Multimodal Treatment Study of Children with ADHD (MTA) was a National Institute of Mental Health (NIMH) cooperative agreement randomized clinical trial, continued under an NIMH contract as a follow-up study and finally under a National Institute on Drug Abuse (NIDA) contract followed by a data analysis grant (DA039881). The Spanish sample was recruited, assessed and genotyped using funds from the Instituto de Salud Carlos III, Spain (PI12/01139, PI14/01700, PI15/01789, PI16/01505), and co-financed by the European Regional Development Fund (ERDF); Agència de Gestió d’Ajuts Universitaris i de Recerca-AGAUR, Generalitat de Catalunya (2014SGR1357, 2014SGR0932); Departament de Salut, Generalitat de Catalunya; Ministerio de Economía, Industria y Competitividad, Spain (SAF2015-68341-R); the European College of Neuropsychopharmacology (ECNP network: ‘ADHD across the lifespan’) and a NARSAD Young Investigator Grant from the Brain & Behavior Research Foundation. This project has also received funding from the European Union’s Horizon 2020 research and innovation programme (CoCA under grant agreement 667302). C.S.-M. is recipient of a Sara Borrell contract from the Instituto de Salud Carlos III, Ministerio de Economía, Industria y Competitividad, Spain (CD15/00199). M.R. is a recipient of a Miguel de Servet contract from the Instituto de Salud Carlos III, Ministerio de Economía, Industria y Competitividad, Spain (CP09/00119 and CPII15/00023). N.F.-C. was supported by a contract of the Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER).

Related Content

Supplementary information accompanies this paper at: https://doi.org/ 10.1038/s41398-019-0396-7

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