Quantitative trait locus analysis of nonverbal communication in autism spectrum disorder.

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Title: Quantitative trait locus analysis of nonverbal communication in autism spectrum disorder.
Authors: Chen, G. K., Kono, N., Geschwind, D. H., Cantor, R. M.
Source: Molecular Psychiatry. Feb2006, Vol. 11 Issue 2, p214-220. 7p. 5 Charts, 2 Graphs.
Subjects: Autism, Nonverbal communication, Developmental disabilities, Interpersonal communication, Neurodevelopmental treatment, Genetic disorders, Familial diseases, Medical genetics
Abstract: Autism spectrum disorder (ASD) is a neurodevelopmental syndrome marked by impairments in social interactive functioning and communication skills, and the presence of repetitive and restrictive behaviors. Twin and linkage studies provide evidence that ASD is heritable and genetically complex. Genetic analyses of familial quantitative traits in those with ASD may help to reveal underlying risk genes. We report a quantitative trait locus (QTL) analysis of nonverbal communication (NVC) in 228 families from the autism genetics resource exchange (AGRE) ascertained for at least two siblings with ASD. QTL at 1p13–q12, 4q21–25, 7q35, 8q23–24, and 16p12–13 indicate that genes at these loci may contribute to the variation in NVC among those with ASD. Using the criteria of Lander and Kruglyak, the QTL at 1p13–q12 is ‘suggestive’, while the other four are ‘possible’. To assess whether these QTL are likely to harbor genes contributing specifically to the deficits in NVC, linkage analysis of ASD sibships with the most severe NVC scores was conducted. The sibships were identified by ordered-subset analyses (OSA), and families with the most severe NVC scores displayed lod scores of 3.4 at 8q23–24 and 3.8 at 16p12–13, indicating that these two regions are likely to harbor gene(s) contributing to ASD by predisposing to deficits in NVC.Molecular Psychiatry (2006) 11, 214–220. doi:10.1038/sj.mp.4001753; published online 27 September 2005 [ABSTRACT FROM AUTHOR]
Copyright of Molecular Psychiatry 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.)
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  Data: <searchLink fieldCode="AR" term="%22Chen%2C+G%2E+K%2E%22">Chen, G. K.</searchLink><br /><searchLink fieldCode="AR" term="%22Kono%2C+N%2E%22">Kono, N.</searchLink><br /><searchLink fieldCode="AR" term="%22Geschwind%2C+D%2E+H%2E%22">Geschwind, D. H.</searchLink><br /><searchLink fieldCode="AR" term="%22Cantor%2C+R%2E+M%2E%22">Cantor, R. M.</searchLink>
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  Data: <searchLink fieldCode="JN" term="%22Molecular+Psychiatry%22">Molecular Psychiatry</searchLink>. Feb2006, Vol. 11 Issue 2, p214-220. 7p. 5 Charts, 2 Graphs.
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  Data: Autism spectrum disorder (ASD) is a neurodevelopmental syndrome marked by impairments in social interactive functioning and communication skills, and the presence of repetitive and restrictive behaviors. Twin and linkage studies provide evidence that ASD is heritable and genetically complex. Genetic analyses of familial quantitative traits in those with ASD may help to reveal underlying risk genes. We report a quantitative trait locus (QTL) analysis of nonverbal communication (NVC) in 228 families from the autism genetics resource exchange (AGRE) ascertained for at least two siblings with ASD. QTL at 1p13–q12, 4q21–25, 7q35, 8q23–24, and 16p12–13 indicate that genes at these loci may contribute to the variation in NVC among those with ASD. Using the criteria of Lander and Kruglyak, the QTL at 1p13–q12 is ‘suggestive’, while the other four are ‘possible’. To assess whether these QTL are likely to harbor genes contributing specifically to the deficits in NVC, linkage analysis of ASD sibships with the most severe NVC scores was conducted. The sibships were identified by ordered-subset analyses (OSA), and families with the most severe NVC scores displayed lod scores of 3.4 at 8q23–24 and 3.8 at 16p12–13, indicating that these two regions are likely to harbor gene(s) contributing to ASD by predisposing to deficits in NVC.Molecular Psychiatry (2006) 11, 214–220. doi:10.1038/sj.mp.4001753; published online 27 September 2005 [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Molecular Psychiatry 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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