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Linkage analyses of chromosomal region 18p11-q12 in dyslexia
Institut für Humangenetik, Universität Bonn, Germany.
Institut für Medizinische Biometrie und Statistik, Universitätsklinikum Schleswig-Holstein, Universität Zu Lübeck, Lübeck, Germany .
Klinik und Poliklinik für Kinder- und Jugendpsychiatrie, Julius-Maximilians-Universität Würzburg, Würzburg, Germany.
Institut für Humangenetik, Universität Bonn, Germany.
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2006 (English)In: Journal of neural transmission, ISSN 0300-9564, E-ISSN 1435-1463, Vol. 113, no 3, p. 417-23Article in journal (Refereed) Published
Abstract [en]

Dyslexia is characterized as a significant impairment in reading and spelling ability that cannot be explained by low intelligence, low school attendance or deficits in sensory acuity. It is known to be a hereditary disorder that affects about 5% of school aged children, making it the most common of childhood learning disorders. Several susceptibility loci have been reported on chromosomes 1, 2, 3, 6, 15, and 18. The locus on chromosome 18 has been described as having the strongest influence on single word reading, phoneme awareness, and orthographic coding in the largest genome wide linkage study published to date (Fisher et al., 2002). Here we present data from 82 German families in order to investigate linkage of various dyslexia-related traits to the previously described region on chromosome 18p11-q12. Using two- and multipoint analyses, we did not find support for linkage of spelling, single word reading, phoneme awareness, orthographic coding and rapid naming to any of the 14 genotyped STR markers. Possible explanations for our non-replication include differences in study design, limited power of our study and overestimation of the effect of the chromosome 18 locus in the original study.

Place, publisher, year, edition, pages
Vienna, Austria, 2006. Vol. 113, no 3, p. 417-23
Keywords [en]
Linkage analysis, dyslexia, chromosome 18
National Category
Genetics
Identifiers
URN: urn:nbn:se:oru:diva-40721DOI: 10.1007/s00702-005-0336-yISI: 000235114800014PubMedID: 16075186Scopus ID: 2-s2.0-32044457133OAI: oai:DiVA.org:oru-40721DiVA, id: diva2:778529
Available from: 2015-01-10 Created: 2015-01-10 Last updated: 2018-01-30Bibliographically approved

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Repsilber, Dirk

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