TY - JOUR
T1 - Strong genetic evidence of DCDC2 as a susceptibility gene for dyslexia
AU - Schumacher, Johannes
AU - Anthoni, Heidi
AU - Dahdouh, Faten
AU - König, Inke R.
AU - Hillmer, Axel M.
AU - Kluck, Nadine
AU - Manthey, Malou
AU - Plume, Ellen
AU - Warnke, Andreas
AU - Remschmidt, Helmut
AU - Hülsmann, Jutta
AU - Cichon, Sven
AU - Lindgren, Cecilia M.
AU - Propping, Peter
AU - Zucchelli, Marco
AU - Ziegler, Andreas
AU - Peyrard-Janvid, Myriam
AU - Schulte-Körne, Gerd
AU - Nöthen, Markus M.
AU - Kere, Juha
N1 - Funding Information:
We are grateful to all investigated individuals for their cooperation in this study. This study was supported by the Deutsche Forschungsgemeinschaft. P.P. was supported by the National Genomic Network of the Bundesministerium für Bildung und Forschung. M.M.N. received support for this work from the Alfried Krupp von Bohlen und Halbach-Stiftung. M.P.-J. is a recipient of a research position from the Swedish Research Council (Vetenskpsrådet). J.K. is supported by grants from the Swedish Research Council, the Academy of Finland, the Sigrid Jusélius Foundation, and the Päivikki and Sakari Sohlberg Foundation. Some of the results were obtained by using the program package S.A.G.E., which is supported by U.S. Public Health Service Resource grant RR03655 from the National Center for Research Resources.
PY - 2006/1
Y1 - 2006/1
N2 - We searched for linkage disequilibrium (LD) in 137 triads with dyslexia, using markers that span the most-replicated dyslexia susceptibility region on 6p21-p22, and found association between the disease and markers within the VMP/DCDC2/KAAG1 locus. Detailed refinement of the LD region, involving sequencing and genotyping of additional markers, showed significant association within DCDC2 in single-marker and haplotype analyses. The association appeared to be strongest in severely affected patients. In a second step, the study was extended to include an independent sample of 239 triads with dyslexia, in which the association-in particular, with the severe phenotype of dyslexia-was confirmed. Our expression data showed that DCDC2, which contains a doublecortin homology domain that is possibly involved in cortical neuron migration, is expressed in the fetal and adult CNS, which-together with the hypothesized protein function-is in accordance with findings in dyslexic patients with abnormal neuronal migration and maturation.
AB - We searched for linkage disequilibrium (LD) in 137 triads with dyslexia, using markers that span the most-replicated dyslexia susceptibility region on 6p21-p22, and found association between the disease and markers within the VMP/DCDC2/KAAG1 locus. Detailed refinement of the LD region, involving sequencing and genotyping of additional markers, showed significant association within DCDC2 in single-marker and haplotype analyses. The association appeared to be strongest in severely affected patients. In a second step, the study was extended to include an independent sample of 239 triads with dyslexia, in which the association-in particular, with the severe phenotype of dyslexia-was confirmed. Our expression data showed that DCDC2, which contains a doublecortin homology domain that is possibly involved in cortical neuron migration, is expressed in the fetal and adult CNS, which-together with the hypothesized protein function-is in accordance with findings in dyslexic patients with abnormal neuronal migration and maturation.
UR - http://www.scopus.com/inward/record.url?scp=29244468273&partnerID=8YFLogxK
U2 - 10.1086/498992
DO - 10.1086/498992
M3 - Journal articles
C2 - 16385449
AN - SCOPUS:29244468273
VL - 78
SP - 52
EP - 62
JO - Am. J. Hum. Genet.
JF - Am. J. Hum. Genet.
SN - 0002-9297
IS - 1
ER -
