BRIEF REPORTSInvestigation of the DCDC2 intron 2 deletion/compound short tandem repeat polymorphism in a large German dyslexia sampleLudwig, Kerstin U.a; Schumacher, Johannesb; Schulte-Körne, Gerdc; König, Inke R.e; Warnke, Andreasf; Plume, Ellenf; Anthoni, Heidih; Peyrard-Janvid, Myriamh; Meng, Haiyingi; Ziegler, Andrease; Remschmidt, Helmutg; Kere, Juhah; Gruen, Jeffrey R.i; Müller-Myhsok, Bertramd; Nöthen, Markus M.a; Hoffmann, PeraAuthor Information aDepartment of Genomics, Life and Brain Center bInstitute of Human Genetics, University of Bonn, Bonn cDepartment of Child and Adolescent Psychiatry and Psychotherapy, University Hospital Munich dMax-Planck Institute of Psychiatry, Munich eInstitute of Medical Biometry and Statistics, University Hospital Schleswig-Holstein-Campus Lübeck, Lübeck fDepartment of Child and Adolescent Psychiatry and Psychotherapy, University of Würzburg, Würzburg gDepartment of Child and Adolescent Psychiatry and Psychotherapy, University of Marburg, Marburg, Germany hDepartment of Biosciences and Nutrition, and Clinical Research Center, Karolinska Institute, Stockholm, Sweden iDepartments of Pediatrics, Genetics, and Investigative Medicine, Yale Child Health Research Center, Yale University School of Medicine, New Haven, USA Correspondence to Per Hoffmann, Department of Genomics, Life and Brain Center, University of Bonn, Sigmund-Freud-Str. 25, D-53105 Bonn, Germany Tel: +49 228 6885427; fax: +49 228 6885401; e-mail: [email protected] Received 26 April 2007 Revised 29 August 2007 Accepted 9 March 2008 Psychiatric Genetics: December 2008 - Volume 18 - Issue 6 - p 310-312 doi: 10.1097/YPG.0b013e3283063a78 Buy Metrics Abstract Dyslexia is a complex disorder manifested by difficulties in learning to read and spell despite conventional instruction, adequate intelligence and sociocultural opportunity. It is among the most common neurodevelopmental disorders with a prevalence of 5–12%. The dyslexia susceptibility locus 2 on chromosome 6p21–p22 is one of the best-replicated linkage regions in dyslexia. On the basis of systematic linkage disequilibrium studies, the doublecortin domain containing protein 2 gene (DCDC2) was identified as a strong candidate gene in this region. Data from a US study have suggested a complex deletion/compound short tandem repeat (STR) polymorphism in intron 2 of DCDC2 as the causative mutation. In this study, we analyzed this polymorphism in 396 German dyslexia trios which included 376 trios previously providing strong support for the DCDC2 locus. We observed no significant deviation from random transmission, neither for the deletion nor for the alleles of the compound STR. We also did not find the deletion or any of the STR alleles to be in linkage disequilibrium with the 2-marker haplotype, which was associated with dyslexia in our sample. We thus conclude that the causative variant/s in DCDC2 conferring susceptibility to dyslexia in our sample remain/s to be identified. © 2008 Lippincott Williams & Wilkins, Inc.