Genome-wide association scan identifies new variants associated with a cognitive predictor of dyslexia View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-02-11

AUTHORS

Alessandro Gialluisi, Till F. M. Andlauer, Nazanin Mirza-Schreiber, Kristina Moll, Jessica Becker, Per Hoffmann, Kerstin U. Ludwig, Darina Czamara, Beate St Pourcain, William Brandler, Ferenc Honbolygó, Dénes Tóth, Valéria Csépe, Guillaume Huguet, Andrew P. Morris, Jacqueline Hulslander, Erik G. Willcutt, John C. DeFries, Richard K. Olson, Shelley D. Smith, Bruce F. Pennington, Anniek Vaessen, Urs Maurer, Heikki Lyytinen, Myriam Peyrard-Janvid, Paavo H. T. Leppänen, Daniel Brandeis, Milene Bonte, John F. Stein, Joel B. Talcott, Fabien Fauchereau, Arndt Wilcke, Clyde Francks, Thomas Bourgeron, Anthony P. Monaco, Franck Ramus, Karin Landerl, Juha Kere, Thomas S. Scerri, Silvia Paracchini, Simon E. Fisher, Johannes Schumacher, Markus M. Nöthen, Bertram Müller-Myhsok, Gerd Schulte-Körne

ABSTRACT

Developmental dyslexia (DD) is one of the most prevalent learning disorders, with high impact on school and psychosocial development and high comorbidity with conditions like attention-deficit hyperactivity disorder (ADHD), depression, and anxiety. DD is characterized by deficits in different cognitive skills, including word reading, spelling, rapid naming, and phonology. To investigate the genetic basis of DD, we conducted a genome-wide association study (GWAS) of these skills within one of the largest studies available, including nine cohorts of reading-impaired and typically developing children of European ancestry (N = 2562-3468). We observed a genome-wide significant effect (p < 1 × 10-8) on rapid automatized naming of letters (RANlet) for variants on 18q12.2, within MIR924HG (micro-RNA 924 host gene; rs17663182 p = 4.73 × 10-9), and a suggestive association on 8q12.3 within NKAIN3 (encoding a cation transporter; rs16928927, p = 2.25 × 10-8). rs17663182 (18q12.2) also showed genome-wide significant multivariate associations with RAN measures (p = 1.15 × 10-8) and with all the cognitive traits tested (p = 3.07 × 10-8), suggesting (relational) pleiotropic effects of this variant. A polygenic risk score (PRS) analysis revealed significant genetic overlaps of some of the DD-related traits with educational attainment (EDUyears) and ADHD. Reading and spelling abilities were positively associated with EDUyears (p ~ [10-5-10-7]) and negatively associated with ADHD PRS (p ~ [10-8-10-17]). This corroborates a long-standing hypothesis on the partly shared genetic etiology of DD and ADHD, at the genome-wide level. Our findings suggest new candidate DD susceptibility genes and provide new insights into the genetics of dyslexia and its comorbities. More... »

PAGES

77

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  • Journal

    TITLE

    Translational Psychiatry

    ISSUE

    1

    VOLUME

    9

    Author Affiliations

  • Department of Epidemiology and Prevention, IRCCS Istituto Neurologico Mediterraneo Neuromed, Pozzilli, Italy
  • Munich Cluster for Systems Neurology (Sypartially), Munich, Germany
  • Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany
  • Department of Child and Adolescent Psychiatry, Psychosomatic, and Psychotherapy, Ludwig-Maximilians University, Munich, Germany
  • Department of Genomics, Life & Brain Center, University of Bonn, Bonn, Germany
  • MRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK
  • University of California San Diego, Department of Psychiatry, San Diego, CA USA
  • Brain Imaging Centre, Research Centre of Natural Sciences of the Hungarian Academy of Sciences, Budapest, Hungary
  • University Paris Diderot, Sorbonne Paris Cité, Paris, France
  • Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK
  • Institute for Behavioral Genetics and Department of Psychology and Neuroscience, University of Colorado Boulder, Boulder, CO USA
  • Developmental Neuroscience Munroe-Meyer Institute, University of Nebraska Medical Center, Omaha, NE USA
  • Developmental Neuropsychology Lab & Clinic, Department of Psychology, University of Denver, Denver, CO USA
  • Department of Cognitive Neuroscience, Faculty of Psychology and Neuroscience & Maastricht Brain Imaging Center (M-BIC), Maastricht University, Maastricht, Netherlands
  • Department of Psychology, The Chinese University of Hong Kong, Shatin, N.T. Hong Kong
  • Centre for Research on Learning and Teaching, Department of Psychology, University of Jyväskylä, Jyväskylä, Finland
  • Department of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden
  • Neuroscience Center Zurich, University of Zurich and ETH Zurich, Zurich, Switzerland
  • Department of Physiology, University of Oxford, Oxford, UK
  • School of Life and Health Sciences, Aston University, Birmingham, UK
  • Cognitive Genetics Unit, Fraunhofer Institute for Cell Therapy and Immunology, Leipzig, Germany
  • Donders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, Netherlands
  • Tufts University, Medford, MA USA
  • Laboratoire de Sciences Cognitives et Psycholinguistique, Ecole Normale Supérieure, CNRS, EHESS, PSL Research University, Paris, France
  • Institute of Psychology, University of Graz, Graz, Austria and BioTechMed, Graz, Austria
  • School of Basic and Medical Biosciences, King’s College London, London, UK
  • The Walter and Eliza Hall Institute of Medical Research & Melbourne University, Melbourne, Australia
  • School of Medicine, University of St Andrews, St Andrews, UK
  • Institute of Translational Medicine, University of Liverpool, Liverpool, UK
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41398-019-0402-0

    DOI

    http://dx.doi.org/10.1038/s41398-019-0402-0

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1112057092

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30741946


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