Autor: |
Nicole E. Neef, Bent Müller, Johanna Liebig, Gesa Schaadt, Maren Grigutsch, Thomas C. Gunter, Arndt Wilcke, Holger Kirsten, Michael A. Skeide, Indra Kraft, Nina Kraus, Frank Emmrich, Jens Brauer, Johannes Boltze, Angela D. Friederici |
Jazyk: |
angličtina |
Rok vydání: |
2017 |
Předmět: |
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Zdroj: |
Developmental Cognitive Neuroscience, Vol 24, Iss , Pp 63-71 (2017) |
Druh dokumentu: |
article |
ISSN: |
1878-9293 |
DOI: |
10.1016/j.dcn.2017.01.008 |
Popis: |
Dyslexia is a reading disorder with strong associations with KIAA0319 and DCDC2. Both genes play a functional role in spike time precision of neurons. Strikingly, poor readers show an imprecise encoding of fast transients of speech in the auditory brainstem. Whether dyslexia risk genes are related to the quality of sound encoding in the auditory brainstem remains to be investigated. Here, we quantified the response consistency of speech-evoked brainstem responses to the acoustically presented syllable [da] in 159 genotyped, literate and preliterate children. When controlling for age, sex, familial risk and intelligence, partial correlation analyses associated a higher dyslexia risk loading with KIAA0319 with noisier responses. In contrast, a higher risk loading with DCDC2 was associated with a trend towards more stable responses. These results suggest that unstable representation of sound, and thus, reduced neural discrimination ability of stop consonants, occurred in genotypes carrying a higher amount of KIAA0319 risk alleles. Current data provide the first evidence that the dyslexia-associated gene KIAA0319 can alter brainstem responses and impair phoneme processing in the auditory brainstem. This brain-gene relationship provides insight into the complex relationships between phenotype and genotype thereby improving the understanding of the dyslexia-inherent complex multifactorial condition. Keywords: Developmental dyslexia, KIAA0319, DCDC2, Brainstem responses, Sound processing, Genetic risk |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
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