| Literature DB >> 24022301 |
Jessica Becker1, Darina Czamara2, Tom S Scerri3, Franck Ramus4, Valéria Csépe5, Joel B Talcott6, John Stein7, Andrew Morris8, Kerstin U Ludwig1, Per Hoffmann9, Ferenc Honbolygó5, Dénes Tóth5, Fabien Fauchereau10, Caroline Bogliotti4, Stéphanie Iannuzzi11, Yves Chaix12, Sylviane Valdois13, Catherine Billard14, Florence George15, Isabelle Soares-Boucaud16, Christophe-Loïc Gérard17, Sanne van der Mark18, Enrico Schulz19, Anniek Vaessen20, Urs Maurer21, Kaisa Lohvansuu22, Heikki Lyytinen22, Marco Zucchelli23, Daniel Brandeis24, Leo Blomert20, Paavo H T Leppänen22, Jennifer Bruder25, Anthony P Monaco8, Bertram Müller-Myhsok2, Juha Kere26, Karin Landerl27, Markus M Nöthen1, Gerd Schulte-Körne25, Silvia Paracchini28, Myriam Peyrard-Janvid23, Johannes Schumacher29.
Abstract
Dyslexia is one of the most common childhood disorders with a prevalence of around 5-10% in school-age children. Although an important genetic component is known to have a role in the aetiology of dyslexia, we are far from understanding the molecular mechanisms leading to the disorder. Several candidate genes have been implicated in dyslexia, including DYX1C1, DCDC2, KIAA0319, and the MRPL19/C2ORF3 locus, each with reports of both positive and no replications. We generated a European cross-linguistic sample of school-age children - the NeuroDys cohort - that includes more than 900 individuals with dyslexia, sampled with homogenous inclusion criteria across eight European countries, and a comparable number of controls. Here, we describe association analysis of the dyslexia candidate genes/locus in the NeuroDys cohort. We performed both case-control and quantitative association analyses of single markers and haplotypes previously reported to be dyslexia-associated. Although we observed association signals in samples from single countries, we did not find any marker or haplotype that was significantly associated with either case-control status or quantitative measurements of word-reading or spelling in the meta-analysis of all eight countries combined. Like in other neurocognitive disorders, our findings underline the need for larger sample sizes to validate possibly weak genetic effects.Entities:
Mesh:
Year: 2013 PMID: 24022301 PMCID: PMC3992562 DOI: 10.1038/ejhg.2013.199
Source DB: PubMed Journal: Eur J Hum Genet ISSN: 1018-4813 Impact factor: 4.246