A family based study implicates solute carrier family 1-member 3 (SLC1A3) gene in attention-deficit/hyperactivity disorder

Darko Turic; Kate Langley; Hywel Williams; Nadine Norton; Nigel M. Williams; Valentina Moskvina; Marianne B. Van Den Bree; Michael J. Owen; Anita Thapar; Michael C. O'Donovan

doi:10.1016/j.biopsych.2005.03.025

A family based study implicates solute carrier family 1-member 3 (SLC1A3) gene in attention-deficit/hyperactivity disorder

Darko Turic, Kate Langley, Hywel Williams, Nadine Norton, Nigel M. Williams, Valentina Moskvina, Marianne B. Van Den Bree, Michael J. Owen, Anita Thapar, Michael C. O'Donovan

Cancer Biology

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24 Scopus citations

Abstract

Background: The glutamatergic system, the major excitatory neurotransmitter system in the central nervous system (CNS) has been proposed as contributing a possible role in the etiology of attention deficit hyperactivity disorder (ADHD). This is based upon observations from animal, neuroimaging, neuroanatomical and neuropsychological studies. Genes related to glutamate function are therefore good functional candidates for this disorder. The SLC1A3 (Solute Carrier Family 1, member 3) gene encodes a glial glutamate transporter which maps to chromosome 5p12, a region of linkage that coincides in two published ADHD genome scans so far. SLC1A3 is thus both a functional and positional candidate gene for ADHD. Methods: We have undertaken detailed association analysis of SLC1A3 using a multi-stage approach for candidate gene analysis. Results: In a family-based sample (n = 299) we found a significant association between marker rs2269272 (p = .007) and ADHD. Two, two-marker haplotypes, rs2269272/rs3776581 (p = .016) and rs2269272/rs2032893 (p = .013) also yielded evidence of association. Conclusions: The results of our study suggest that genetic variation in SLC1A3 may contribute to susceptibility to ADHD.

Original language	English (US)
Pages (from-to)	1461-1466
Number of pages	6
Journal	Biological psychiatry
Volume	57
Issue number	11
DOIs	https://doi.org/10.1016/j.biopsych.2005.03.025
State	Published - Jun 1 2005

Keywords

Attention deficit hyperactivity disorder (ADHD)
Glutamate function
Haplotype
Polymorphisms
SLC1A3

ASJC Scopus subject areas

Biological Psychiatry

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10.1016/j.biopsych.2005.03.025

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@article{f8f36e075377445cb99b76f2b502a14e,

title = "A family based study implicates solute carrier family 1-member 3 (SLC1A3) gene in attention-deficit/hyperactivity disorder",

abstract = "Background: The glutamatergic system, the major excitatory neurotransmitter system in the central nervous system (CNS) has been proposed as contributing a possible role in the etiology of attention deficit hyperactivity disorder (ADHD). This is based upon observations from animal, neuroimaging, neuroanatomical and neuropsychological studies. Genes related to glutamate function are therefore good functional candidates for this disorder. The SLC1A3 (Solute Carrier Family 1, member 3) gene encodes a glial glutamate transporter which maps to chromosome 5p12, a region of linkage that coincides in two published ADHD genome scans so far. SLC1A3 is thus both a functional and positional candidate gene for ADHD. Methods: We have undertaken detailed association analysis of SLC1A3 using a multi-stage approach for candidate gene analysis. Results: In a family-based sample (n = 299) we found a significant association between marker rs2269272 (p = .007) and ADHD. Two, two-marker haplotypes, rs2269272/rs3776581 (p = .016) and rs2269272/rs2032893 (p = .013) also yielded evidence of association. Conclusions: The results of our study suggest that genetic variation in SLC1A3 may contribute to susceptibility to ADHD.",

keywords = "Attention deficit hyperactivity disorder (ADHD), Glutamate function, Haplotype, Polymorphisms, SLC1A3",

author = "Darko Turic and Kate Langley and Hywel Williams and Nadine Norton and Williams, {Nigel M.} and Valentina Moskvina and {Van Den Bree}, {Marianne B.} and Owen, {Michael J.} and Anita Thapar and O'Donovan, {Michael C.}",

note = "Funding Information: This work has been funded by the Wellcome Trust, Action Research and Sport Aiding Medical Research for Kids. Thanks to Deborah Lawson, Sophie Mills, Helen Pay, Jane Holmes, Tracey Hever, Richard Harrington, Tony Payton, Jane Worthington and Bill Ollier who were involved in sample collection and the first wave of this study. We thank all the clinicians who supported this work and are especially grateful to all the families who participated in this study. Copyright: Copyright 2008 Elsevier B.V., All rights reserved.",

year = "2005",

month = jun,

day = "1",

doi = "10.1016/j.biopsych.2005.03.025",

language = "English (US)",

volume = "57",

pages = "1461--1466",

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T1 - A family based study implicates solute carrier family 1-member 3 (SLC1A3) gene in attention-deficit/hyperactivity disorder

AU - Turic, Darko

AU - Langley, Kate

AU - Williams, Hywel

AU - Norton, Nadine

AU - Williams, Nigel M.

AU - Moskvina, Valentina

AU - Van Den Bree, Marianne B.

AU - Owen, Michael J.

AU - Thapar, Anita

AU - O'Donovan, Michael C.

N1 - Funding Information: This work has been funded by the Wellcome Trust, Action Research and Sport Aiding Medical Research for Kids. Thanks to Deborah Lawson, Sophie Mills, Helen Pay, Jane Holmes, Tracey Hever, Richard Harrington, Tony Payton, Jane Worthington and Bill Ollier who were involved in sample collection and the first wave of this study. We thank all the clinicians who supported this work and are especially grateful to all the families who participated in this study. Copyright: Copyright 2008 Elsevier B.V., All rights reserved.

PY - 2005/6/1

Y1 - 2005/6/1

N2 - Background: The glutamatergic system, the major excitatory neurotransmitter system in the central nervous system (CNS) has been proposed as contributing a possible role in the etiology of attention deficit hyperactivity disorder (ADHD). This is based upon observations from animal, neuroimaging, neuroanatomical and neuropsychological studies. Genes related to glutamate function are therefore good functional candidates for this disorder. The SLC1A3 (Solute Carrier Family 1, member 3) gene encodes a glial glutamate transporter which maps to chromosome 5p12, a region of linkage that coincides in two published ADHD genome scans so far. SLC1A3 is thus both a functional and positional candidate gene for ADHD. Methods: We have undertaken detailed association analysis of SLC1A3 using a multi-stage approach for candidate gene analysis. Results: In a family-based sample (n = 299) we found a significant association between marker rs2269272 (p = .007) and ADHD. Two, two-marker haplotypes, rs2269272/rs3776581 (p = .016) and rs2269272/rs2032893 (p = .013) also yielded evidence of association. Conclusions: The results of our study suggest that genetic variation in SLC1A3 may contribute to susceptibility to ADHD.

AB - Background: The glutamatergic system, the major excitatory neurotransmitter system in the central nervous system (CNS) has been proposed as contributing a possible role in the etiology of attention deficit hyperactivity disorder (ADHD). This is based upon observations from animal, neuroimaging, neuroanatomical and neuropsychological studies. Genes related to glutamate function are therefore good functional candidates for this disorder. The SLC1A3 (Solute Carrier Family 1, member 3) gene encodes a glial glutamate transporter which maps to chromosome 5p12, a region of linkage that coincides in two published ADHD genome scans so far. SLC1A3 is thus both a functional and positional candidate gene for ADHD. Methods: We have undertaken detailed association analysis of SLC1A3 using a multi-stage approach for candidate gene analysis. Results: In a family-based sample (n = 299) we found a significant association between marker rs2269272 (p = .007) and ADHD. Two, two-marker haplotypes, rs2269272/rs3776581 (p = .016) and rs2269272/rs2032893 (p = .013) also yielded evidence of association. Conclusions: The results of our study suggest that genetic variation in SLC1A3 may contribute to susceptibility to ADHD.

KW - Attention deficit hyperactivity disorder (ADHD)

KW - Glutamate function

KW - Haplotype

KW - Polymorphisms

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JO - Biological psychiatry

JF - Biological psychiatry

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ER -

A family based study implicates solute carrier family 1-member 3 (SLC1A3) gene in attention-deficit/hyperactivity disorder

Abstract

Keywords

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