Literaturnachweis - Detailanzeige
| Autor/inn/en | Wilcke, A.; Weissfuss, J.; Kirsten, H.; Wolfram, G.; Boltze, J.; Ahnert, P. |
|---|---|
| Titel | The Role of Gene DCDC2 in German Dyslexics |
| Quelle | In: Annals of Dyslexia, 59 (2009) 1, S.1-11 (11 Seiten)Infoseite zur Zeitschrift
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| Sprache | englisch |
| Dokumenttyp | gedruckt; online; Zeitschriftenaufsatz |
| ISSN | 0736-9387 |
| DOI | 10.1007/s11881-008-0020-7 |
| Schlagwörter | Dyslexia; Genetics; Etiology; Genetic Disorders; Foreign Countries; Influences; Correlation; Symptoms (Individual Disorders); Neurological Impairments; Germany |
| Abstract | Dyslexia is a complex reading and writing disorder with a strong genetic component. In a German case-control cohort, we studied the influence of the suspected dyslexia-associated gene DCDC2. For the first time in a German cohort, we describe association of a 2445 basepair deletion, first identified in an American study. Evidence of association for three DCDC2 single nucleotide polymorphisms (rs807724, rs793862, rs807701), previously identified in German or American cohorts, was replicated. A haplotype of these polymorphisms showed evidence for association as well. Thus, our data further corroborate association of DCDC2 with dyslexia. Analysis of functional subgroups suggests association of investigated DCDC2 variants mainly with nondysphonetic, nonsevere, but probably dyseidetic (surface) dyslexia. Based on the presumed function of DCDC2, our findings point to a role of impaired neuronal migration in the etiology of the disease. (As Provided). |
| Anmerkungen | Springer. 233 Spring Street, New York, NY 10013. Tel: 800-777-4643; Tel: 212-460-1500; Fax: 212-348-4505; e-mail: service-ny@springer.com; Web site: http://www.springerlink.com |
| Erfasst von | ERIC (Education Resources Information Center), Washington, DC |
| Update | 2017/4/10 |
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