Evidence of linkage between the serotonin transporter and autistic disorder

被引：0

作者：

Cook Jr. E.H. ^{[1
,5
]}

Courchesne R. ^{[2
]}

Lord C. ^{[2
]}

Cox N.J. ^{[3
]}

Van S. ^{[1
]}

Lincoln A. ^{[2
]}

Haas R. ^{[2
]}

Courchesne E. ^{[2
,4
]}

Leventhal B.L. ^{[1
]}

机构：

[1] Lab. of Developmental Neuroscience, Department of Psychiatry, University of Chicago, Chicago, IL 60637

[2] Autism/Brain Devmt. Res. Laboratory, Children's Hospital, Research Center, San Diego, CA 92037

[3] Department of Medicine, University of Chicago, Chicago, IL 60637

[4] Neuroscience Department, School of Medicine, Univ. of California at San Diego, San Diego

[5] MC 3077, University of Chicago, Chicago, IL 60637

来源：

Molecular Psychiatry | 1997年 / 2卷 / 3期

关键词：

Autism; Infantile; Linkage; Linkage disequilibrium; Monoamines; Polymorphism; Promoter; Serotonin; Transporter;

D O I：

10.1038/sj.mp.4000266

中图分类号：

学科分类号：

摘要：

The serotonin transporter gene (HTT) is a primary candidate in autistic disorder based on efficacy of potent serotonin transporter inhibitors in reducing rituals and routines. We initiated a candidate gene study of HTT in trios consisting of probands with autistic disorder and both parents. Preliminary transmission/disequilibrium test (TDT) analysis with 86 families revealed no evidence for linkage or linkage disequilibrium between autistic disorder and a polymorphism in the second intron of HTT. However, preferential transmission of a short variant of the HTT promoter was found in the same 86 trios (TDT χ2 = 4.69, 1 d.f., P = 0.030). In further analyses, we considered haplotypes of the HTT promoter variant and second intron locus as alleles in a multiallelic TDT. Results confirmed the significance of the effect of this region (TDT χ2 = 11.85, 4 d.f., P = 0.018). This provides preliminary evidence of linkage and association between HTT and autistic disorder.

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页码：247 / 250

页数：3

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