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Investigation of Dyslexia and SLI Risk Variants in Reading- and Language-Impaired Subjects.

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Title: Investigation of Dyslexia and SLI Risk Variants in Reading- and Language-Impaired Subjects.
Authors: Newbury, D. F., Paracchini, S., Scerri, T. S., Winchester, L., Addis, L., Richardson, Alex J., Walter, J., Stein, J. F., Talcott, J. B., Monaco, A. P.
Source: Behavior Genetics. Jan2011, Vol. 41 Issue 1, p90-104. 15p. 4 Charts.
Subjects: Dyslexia, Specific language impairment in children, Learning disability genetics, Linkage (Genetics), Cohort analysis
Abstract: Dyslexia (or reading disability) and specific language impairment (or SLI) are common childhood disorders that show considerable co-morbidity and diagnostic overlaps and have been suggested to share some genetic aetiology. Recently, genetic risk variants have been identified for SLI and dyslexia enabling the direct evaluation of possible shared genetic influences between these disorders. In this study we investigate the role of variants in these genes (namely MRPL19/ C20RF3, ROBO1, DCDC2, KIAA0319, DYX1C1, CNTNAP2, ATP2C2 and CMIP) in the aetiology of SLI and dyslexia. We perform case-control and quantitative association analyses using measures of oral and written language skills in samples of SLI and dyslexic families and cases. We replicate association between KIAA0319 and DCDC2 and dyslexia and provide evidence to support a role for KIAA0319 in oral language ability. In addition, we find association between reading-related measures and variants in CNTNAP2 and CMIP in the SLI families. [ABSTRACT FROM AUTHOR]
Copyright of Behavior Genetics is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Investigation of Dyslexia and SLI Risk Variants in Reading- and Language-Impaired Subjects.
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  Data: <searchLink fieldCode="JN" term="%22Behavior+Genetics%22">Behavior Genetics</searchLink>. Jan2011, Vol. 41 Issue 1, p90-104. 15p. 4 Charts.
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  Data: <searchLink fieldCode="DE" term="%22Dyslexia%22">Dyslexia</searchLink><br /><searchLink fieldCode="DE" term="%22Specific+language+impairment+in+children%22">Specific language impairment in children</searchLink><br /><searchLink fieldCode="DE" term="%22Learning+disability+genetics%22">Learning disability genetics</searchLink><br /><searchLink fieldCode="DE" term="%22Linkage+%28Genetics%29%22">Linkage (Genetics)</searchLink><br /><searchLink fieldCode="DE" term="%22Cohort+analysis%22">Cohort analysis</searchLink>
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  Data: Dyslexia (or reading disability) and specific language impairment (or SLI) are common childhood disorders that show considerable co-morbidity and diagnostic overlaps and have been suggested to share some genetic aetiology. Recently, genetic risk variants have been identified for SLI and dyslexia enabling the direct evaluation of possible shared genetic influences between these disorders. In this study we investigate the role of variants in these genes (namely MRPL19/ C20RF3, ROBO1, DCDC2, KIAA0319, DYX1C1, CNTNAP2, ATP2C2 and CMIP) in the aetiology of SLI and dyslexia. We perform case-control and quantitative association analyses using measures of oral and written language skills in samples of SLI and dyslexic families and cases. We replicate association between KIAA0319 and DCDC2 and dyslexia and provide evidence to support a role for KIAA0319 in oral language ability. In addition, we find association between reading-related measures and variants in CNTNAP2 and CMIP in the SLI families. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Behavior Genetics is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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