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First genome-wide association scan on neurophysiological endophenotypes points to trans-regulation effects on SLC2A3 in dyslexic children.

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Title: First genome-wide association scan on neurophysiological endophenotypes points to trans-regulation effects on SLC2A3 in dyslexic children.
Authors: Roeske, D., Ludwig, K. U., Neuhoff, N., Becker, J., Bartling, J., Bruder, J., Brockschmidt, F. F., Warnke, A., Remschmidt, H., Hoffmann, P., Müller-Myhsok, B., Nöthen, M. M., Schulte-Körne, G.
Source: Molecular Psychiatry. Jan2011, Vol. 16 Issue 1, p97-107. 11p. 2 Charts, 2 Graphs.
Subjects: Children with dyslexia, Messenger RNA, Speech disorders, Genetic polymorphisms, Neurons
Abstract: Dyslexia is one of the most common learning disorders affecting about 5% of all school-aged children. It has been shown that event-related potential measurements reveal differences between dyslexic children and age-matched controls. This holds particularly true for mismatch negativity (MMN), which reflects automatic speech deviance processing and is altered in dyslexic children. We performed a whole-genome association analysis in 200 dyslexic children, focusing on MMN measurements. We identified rs4234898, a marker located on chromosome 4q32.1, to be significantly associated with the late MMN component. This association could be replicated in an independent second sample of 186 dyslexic children, reaching genome-wide significance in the combined sample (P=5.14e−08). We also found an association between the late MMN component and a two-marker haplotype of rs4234898 and rs11100040, one of its neighboring single nucleotide polymorphisms (SNPs). In the combined sample, this marker combination withstands correction for multiple testing (P=6.71e−08). Both SNPs lie in a region devoid of any protein-coding genes; however, they both show significant association with mRNA-expression levels of SLC2A3 on chromosome 12, the predominant facilitative glucose transporter in neurons. Our results suggest a possible trans-regulation effect on SLC2A3, which might lead to glucose deficits in dyslexic children and could explain their attenuated MMN in passive listening tasks. [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: First genome-wide association scan on neurophysiological endophenotypes points to trans-regulation effects on SLC2A3 in dyslexic children.
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  Data: <searchLink fieldCode="AR" term="%22Roeske%2C+D%2E%22">Roeske, D.</searchLink><br /><searchLink fieldCode="AR" term="%22Ludwig%2C+K%2E+U%2E%22">Ludwig, K. U.</searchLink><br /><searchLink fieldCode="AR" term="%22Neuhoff%2C+N%2E%22">Neuhoff, N.</searchLink><br /><searchLink fieldCode="AR" term="%22Becker%2C+J%2E%22">Becker, J.</searchLink><br /><searchLink fieldCode="AR" term="%22Bartling%2C+J%2E%22">Bartling, J.</searchLink><br /><searchLink fieldCode="AR" term="%22Bruder%2C+J%2E%22">Bruder, J.</searchLink><br /><searchLink fieldCode="AR" term="%22Brockschmidt%2C+F%2E+F%2E%22">Brockschmidt, F. F.</searchLink><br /><searchLink fieldCode="AR" term="%22Warnke%2C+A%2E%22">Warnke, A.</searchLink><br /><searchLink fieldCode="AR" term="%22Remschmidt%2C+H%2E%22">Remschmidt, H.</searchLink><br /><searchLink fieldCode="AR" term="%22Hoffmann%2C+P%2E%22">Hoffmann, P.</searchLink><br /><searchLink fieldCode="AR" term="%22Müller-Myhsok%2C+B%2E%22">Müller-Myhsok, B.</searchLink><br /><searchLink fieldCode="AR" term="%22Nöthen%2C+M%2E+M%2E%22">Nöthen, M. M.</searchLink><br /><searchLink fieldCode="AR" term="%22Schulte-Körne%2C+G%2E%22">Schulte-Körne, G.</searchLink>
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  Data: <searchLink fieldCode="JN" term="%22Molecular+Psychiatry%22">Molecular Psychiatry</searchLink>. Jan2011, Vol. 16 Issue 1, p97-107. 11p. 2 Charts, 2 Graphs.
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  Data: <searchLink fieldCode="DE" term="%22Children+with+dyslexia%22">Children with dyslexia</searchLink><br /><searchLink fieldCode="DE" term="%22Messenger+RNA%22">Messenger RNA</searchLink><br /><searchLink fieldCode="DE" term="%22Speech+disorders%22">Speech disorders</searchLink><br /><searchLink fieldCode="DE" term="%22Genetic+polymorphisms%22">Genetic polymorphisms</searchLink><br /><searchLink fieldCode="DE" term="%22Neurons%22">Neurons</searchLink>
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  Data: Dyslexia is one of the most common learning disorders affecting about 5% of all school-aged children. It has been shown that event-related potential measurements reveal differences between dyslexic children and age-matched controls. This holds particularly true for mismatch negativity (MMN), which reflects automatic speech deviance processing and is altered in dyslexic children. We performed a whole-genome association analysis in 200 dyslexic children, focusing on MMN measurements. We identified rs4234898, a marker located on chromosome 4q32.1, to be significantly associated with the late MMN component. This association could be replicated in an independent second sample of 186 dyslexic children, reaching genome-wide significance in the combined sample (P=5.14e−08). We also found an association between the late MMN component and a two-marker haplotype of rs4234898 and rs11100040, one of its neighboring single nucleotide polymorphisms (SNPs). In the combined sample, this marker combination withstands correction for multiple testing (P=6.71e−08). Both SNPs lie in a region devoid of any protein-coding genes; however, they both show significant association with mRNA-expression levels of SLC2A3 on chromosome 12, the predominant facilitative glucose transporter in neurons. Our results suggest a possible trans-regulation effect on SLC2A3, which might lead to glucose deficits in dyslexic children and could explain their attenuated MMN in passive listening tasks. [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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