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Autism and the serotonin transporter: the long and short of it.

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Title: Autism and the serotonin transporter: the long and short of it.
Authors: Devlin, B., Cook Jr., E. H., Coon, H., Dawson, G., Grigorenko, E. L., McMahon, W., Minshew, N., Pauls, D., Smith, M., Spence, M. A., Rodier, P. M., Stodgell, C., Schellenberg, G. D.
Source: Molecular Psychiatry. Dec2005, Vol. 10 Issue 12, p1110-1116. 7p. 4 Charts.
Subjects: Autism, Autism in children, Diagnosis of autism, Serotonin, Genetics, Developmental disabilities
Abstract: Autism is a neurodevelopmental disorder manifesting early in childhood. Some symptoms of autism are alleviated by treatment with selective serotonin reuptake inhibitors, which are known to interact with the serotonin transporter. Moreover, variation in the gene that encodes the transporter (SLC6A4), especially the HTTLPR locus, is known to modulate its expression. It is natural, therefore, to evaluate whether this variation plays a role in liability to autism. We investigated the impact of alleles at HTTLPR and three other loci in SLC6A4 by using a large, independent family-based sample (390 families, 1528 individuals) from the NIH Collaborative Programs of Excellence in Autism (CPEA) network. Allele transmissions to individuals diagnosed with autism were biased only for HTTLPR, both for the narrow diagnosis of autism (P=0.035) and for the broader diagnosis of autism spectrum (P=0.007). The short allele of HTTLPR was significantly overtransmitted. Investigation of haplotype transmissions suggested that, in our data, biased transmission was only due to HTTLPR. With respect to this locus, there are now seven of 12 studies reporting significant transmission bias of HTTLPR alleles, a noteworthy result in itself. However, the studies with significant findings are almost equally divided between overtransmission of short and overtransmission of long alleles. We place our results within this extremely heterogeneous field of studies. Determining the factors influencing the relationship between autism phenotypes and HTTLPR variation, as well as other loci in SLC6A4, could be an important advance in our understanding of this complex disorder.Molecular Psychiatry (2005) 10, 1110–1116. doi:10.1038/sj.mp.4001724; published online 16 August 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="%22Devlin%2C+B%2E%22">Devlin, B.</searchLink><br /><searchLink fieldCode="AR" term="%22Cook+Jr%2E%2C+E%2E+H%2E%22">Cook Jr., E. H.</searchLink><br /><searchLink fieldCode="AR" term="%22Coon%2C+H%2E%22">Coon, H.</searchLink><br /><searchLink fieldCode="AR" term="%22Dawson%2C+G%2E%22">Dawson, G.</searchLink><br /><searchLink fieldCode="AR" term="%22Grigorenko%2C+E%2E+L%2E%22">Grigorenko, E. L.</searchLink><br /><searchLink fieldCode="AR" term="%22McMahon%2C+W%2E%22">McMahon, W.</searchLink><br /><searchLink fieldCode="AR" term="%22Minshew%2C+N%2E%22">Minshew, N.</searchLink><br /><searchLink fieldCode="AR" term="%22Pauls%2C+D%2E%22">Pauls, D.</searchLink><br /><searchLink fieldCode="AR" term="%22Smith%2C+M%2E%22">Smith, M.</searchLink><br /><searchLink fieldCode="AR" term="%22Spence%2C+M%2E+A%2E%22">Spence, M. A.</searchLink><br /><searchLink fieldCode="AR" term="%22Rodier%2C+P%2E+M%2E%22">Rodier, P. M.</searchLink><br /><searchLink fieldCode="AR" term="%22Stodgell%2C+C%2E%22">Stodgell, C.</searchLink><br /><searchLink fieldCode="AR" term="%22Schellenberg%2C+G%2E+D%2E%22">Schellenberg, G. D.</searchLink>
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  Data: Autism is a neurodevelopmental disorder manifesting early in childhood. Some symptoms of autism are alleviated by treatment with selective serotonin reuptake inhibitors, which are known to interact with the serotonin transporter. Moreover, variation in the gene that encodes the transporter (SLC6A4), especially the HTTLPR locus, is known to modulate its expression. It is natural, therefore, to evaluate whether this variation plays a role in liability to autism. We investigated the impact of alleles at HTTLPR and three other loci in SLC6A4 by using a large, independent family-based sample (390 families, 1528 individuals) from the NIH Collaborative Programs of Excellence in Autism (CPEA) network. Allele transmissions to individuals diagnosed with autism were biased only for HTTLPR, both for the narrow diagnosis of autism (P=0.035) and for the broader diagnosis of autism spectrum (P=0.007). The short allele of HTTLPR was significantly overtransmitted. Investigation of haplotype transmissions suggested that, in our data, biased transmission was only due to HTTLPR. With respect to this locus, there are now seven of 12 studies reporting significant transmission bias of HTTLPR alleles, a noteworthy result in itself. However, the studies with significant findings are almost equally divided between overtransmission of short and overtransmission of long alleles. We place our results within this extremely heterogeneous field of studies. Determining the factors influencing the relationship between autism phenotypes and HTTLPR variation, as well as other loci in SLC6A4, could be an important advance in our understanding of this complex disorder.Molecular Psychiatry (2005) 10, 1110–1116. doi:10.1038/sj.mp.4001724; published online 16 August 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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