A significant association of serotonin transporter polymorphism haplotypes in attention deficit hyperactivity disorder (ADHD)

L. Kent, E. Hardy, Z. Hawi, M Fitzgerald, A. Kirley, Michael Gill, N. Craddock

Research output: Contribution to journalArticleResearchpeer-review

Abstract

Reduced central serotonergic activity has been implicated in poor impulse regulation and aggressive behaviour in animals, adults and also young children. A polymorphism in the promoter of the serotonin transporter (5HTT) has recently been implicated in ADHD. We have examined three 5HTT polymorphisms (the promoter, the VNTR in intron 2 and the 3′ UTR SNP) in a sample of 113 ADHD trios. TDT analysis of haplotypes demonstrated significant preferential transmission of haplotypes containing the T allele of the 3′UTR SNP with the long allele of the promoter polymorphism (2 = 11.96, 3df, p 0.01) and the 10 repeat of the VNTR (2 = 10.18, 4df, P <0.05). A pooled analysis of 289 cases and 372 controls from our, and other published results for the promoter polymorphism demonstrated a significant over-representation of the long allele in ADHD probands compared to controls (2 = 7.14, P <0.01). This study provides further evidence for the possible involvement of the serotonin transporter in susceptibility to ADHD.

Original languageEnglish
Pages (from-to)574-575
Number of pages2
JournalAmerican Journal of Medical Genetics Part B: Neuropsychiatric Genetics
Volume105
Issue number7
Publication statusPublished - 8 Oct 2001
Externally publishedYes

Cite this

@article{c297443d743b4e1388315212e80271a4,
title = "A significant association of serotonin transporter polymorphism haplotypes in attention deficit hyperactivity disorder (ADHD)",
abstract = "Reduced central serotonergic activity has been implicated in poor impulse regulation and aggressive behaviour in animals, adults and also young children. A polymorphism in the promoter of the serotonin transporter (5HTT) has recently been implicated in ADHD. We have examined three 5HTT polymorphisms (the promoter, the VNTR in intron 2 and the 3′ UTR SNP) in a sample of 113 ADHD trios. TDT analysis of haplotypes demonstrated significant preferential transmission of haplotypes containing the T allele of the 3′UTR SNP with the long allele of the promoter polymorphism (2 = 11.96, 3df, p 0.01) and the 10 repeat of the VNTR (2 = 10.18, 4df, P <0.05). A pooled analysis of 289 cases and 372 controls from our, and other published results for the promoter polymorphism demonstrated a significant over-representation of the long allele in ADHD probands compared to controls (2 = 7.14, P <0.01). This study provides further evidence for the possible involvement of the serotonin transporter in susceptibility to ADHD.",
author = "L. Kent and E. Hardy and Z. Hawi and M Fitzgerald and A. Kirley and Michael Gill and N. Craddock",
year = "2001",
month = "10",
day = "8",
language = "English",
volume = "105",
pages = "574--575",
journal = "American Journal of Medical Genetics Part B: Neuropsychiatric Genetics",
issn = "1552-4841",
publisher = "Wiley-Blackwell",
number = "7",

}

A significant association of serotonin transporter polymorphism haplotypes in attention deficit hyperactivity disorder (ADHD). / Kent, L.; Hardy, E.; Hawi, Z.; Fitzgerald, M; Kirley, A.; Gill, Michael; Craddock, N.

In: American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, Vol. 105, No. 7, 08.10.2001, p. 574-575.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - A significant association of serotonin transporter polymorphism haplotypes in attention deficit hyperactivity disorder (ADHD)

AU - Kent, L.

AU - Hardy, E.

AU - Hawi, Z.

AU - Fitzgerald, M

AU - Kirley, A.

AU - Gill, Michael

AU - Craddock, N.

PY - 2001/10/8

Y1 - 2001/10/8

N2 - Reduced central serotonergic activity has been implicated in poor impulse regulation and aggressive behaviour in animals, adults and also young children. A polymorphism in the promoter of the serotonin transporter (5HTT) has recently been implicated in ADHD. We have examined three 5HTT polymorphisms (the promoter, the VNTR in intron 2 and the 3′ UTR SNP) in a sample of 113 ADHD trios. TDT analysis of haplotypes demonstrated significant preferential transmission of haplotypes containing the T allele of the 3′UTR SNP with the long allele of the promoter polymorphism (2 = 11.96, 3df, p 0.01) and the 10 repeat of the VNTR (2 = 10.18, 4df, P <0.05). A pooled analysis of 289 cases and 372 controls from our, and other published results for the promoter polymorphism demonstrated a significant over-representation of the long allele in ADHD probands compared to controls (2 = 7.14, P <0.01). This study provides further evidence for the possible involvement of the serotonin transporter in susceptibility to ADHD.

AB - Reduced central serotonergic activity has been implicated in poor impulse regulation and aggressive behaviour in animals, adults and also young children. A polymorphism in the promoter of the serotonin transporter (5HTT) has recently been implicated in ADHD. We have examined three 5HTT polymorphisms (the promoter, the VNTR in intron 2 and the 3′ UTR SNP) in a sample of 113 ADHD trios. TDT analysis of haplotypes demonstrated significant preferential transmission of haplotypes containing the T allele of the 3′UTR SNP with the long allele of the promoter polymorphism (2 = 11.96, 3df, p 0.01) and the 10 repeat of the VNTR (2 = 10.18, 4df, P <0.05). A pooled analysis of 289 cases and 372 controls from our, and other published results for the promoter polymorphism demonstrated a significant over-representation of the long allele in ADHD probands compared to controls (2 = 7.14, P <0.01). This study provides further evidence for the possible involvement of the serotonin transporter in susceptibility to ADHD.

UR - http://www.scopus.com/inward/record.url?scp=33749098427&partnerID=8YFLogxK

M3 - Article

VL - 105

SP - 574

EP - 575

JO - American Journal of Medical Genetics Part B: Neuropsychiatric Genetics

JF - American Journal of Medical Genetics Part B: Neuropsychiatric Genetics

SN - 1552-4841

IS - 7

ER -