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Angiogenic, neurotrophic, and inflammatory system SNPs moderate the association between birth weight and ADHD symptom severity

Angiogenic, neurotrophic, and inflammatory system SNPs moderate the association between birth weight and ADHD symptom severity
Angiogenic, neurotrophic, and inflammatory system SNPs moderate the association between birth weight and ADHD symptom severity
Low birth weight is associated with increased risk for Attention-Deficit/Hyperactivity Disorder (ADHD); however, the etiological underpinnings of this relationship remain unclear. This study investigated if genetic variants in angiogenic, dopaminergic, neurotrophic, kynurenine, and cytokine-related biological pathways moderate the relationship between birth weight and ADHD symptom severity. A total of 398 youth from two multi-site,
family-based studies of ADHD were included in the analysis. The sample consisted of 360 ADHD probands, 21 affected siblings,and 17 unaffected siblings. A set of 164 SNPs from 31 candidate genes, representing five biological pathways, were included in our analyses. Birth weight and gestational age data were collected from a state birth registry, medical records, and parent report. Generalized Estimating Equations tested for main effects and interactions between individual SNPs and birth weight centile in predicting ADHD symptom severity. SNPs within neurotrophic NTRK3) and cytokine genes (CNTFR) were associated with ADHDinattentive symptomseverity. There was nomain effect of birth weight centile on ADHD symptom severity. SNPs within angiogenic (NRP1 & NRP2), neurotrophic (NTRK1 & NTRK3), cytokine (IL16 & S100B), and kynurenine (CCBL1 & CCBL2) genes moderate the association between birth weight centile and ADHDsymptom severity. The SNPmain effects and SNP?birth weight centile interactions remained significant after adjusting
for multiple testing. Genetic variability in angiogenic, neurotrophic, and inflammatory systems may moderate the association between restricted prenatal growth, a proxy for an adverse prenatal environment, and risk to develop ADHD.
attention deficit hyperactivity disorder, birthweight, gene-environment interaction, neurotrophin, developmental origins of health and disease
1552-4841
691-704
Smith, Taylor F.
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Anastopoulos, Arthur D.
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Garrett, Melanie E.
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Arias-Vasquez, Alejandro
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Franke, Barbara
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Oades, Robert D.
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Sonuga-Barke, Edmund J.S.
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Asherson, Philip
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Gill, Michael
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Buitelaar, Jan K.
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Sergeant, Joseph A.
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Kollins, Scott H.
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Faraone, Stephen V.
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Ashley-Koch, Allison
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Smith, Taylor F.
38952883-a316-4aec-818b-5eb891bdefe9
Anastopoulos, Arthur D.
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Garrett, Melanie E.
2bc52a65-fe91-4b0c-a2e5-5e0ee8328310
Arias-Vasquez, Alejandro
9c3fc332-ff0c-48cd-866c-b2fa8ff074b6
Franke, Barbara
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Oades, Robert D.
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Sonuga-Barke, Edmund J.S.
bc80bf95-6cf9-4c76-a09d-eaaf0b717635
Asherson, Philip
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Gill, Michael
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Buitelaar, Jan K.
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Sergeant, Joseph A.
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Kollins, Scott H.
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Faraone, Stephen V.
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Ashley-Koch, Allison
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Smith, Taylor F., Anastopoulos, Arthur D., Garrett, Melanie E., Arias-Vasquez, Alejandro, Franke, Barbara, Oades, Robert D., Sonuga-Barke, Edmund J.S., Asherson, Philip, Gill, Michael, Buitelaar, Jan K., Sergeant, Joseph A., Kollins, Scott H., Faraone, Stephen V. and Ashley-Koch, Allison (2014) Angiogenic, neurotrophic, and inflammatory system SNPs moderate the association between birth weight and ADHD symptom severity. American Journal of Medical Genetics. Part B: Neuropsychiatric Genetics, 165 (8), 691-704. (doi:10.1002/ajmg.b.32275).

Record type: Article

Abstract

Low birth weight is associated with increased risk for Attention-Deficit/Hyperactivity Disorder (ADHD); however, the etiological underpinnings of this relationship remain unclear. This study investigated if genetic variants in angiogenic, dopaminergic, neurotrophic, kynurenine, and cytokine-related biological pathways moderate the relationship between birth weight and ADHD symptom severity. A total of 398 youth from two multi-site,
family-based studies of ADHD were included in the analysis. The sample consisted of 360 ADHD probands, 21 affected siblings,and 17 unaffected siblings. A set of 164 SNPs from 31 candidate genes, representing five biological pathways, were included in our analyses. Birth weight and gestational age data were collected from a state birth registry, medical records, and parent report. Generalized Estimating Equations tested for main effects and interactions between individual SNPs and birth weight centile in predicting ADHD symptom severity. SNPs within neurotrophic NTRK3) and cytokine genes (CNTFR) were associated with ADHDinattentive symptomseverity. There was nomain effect of birth weight centile on ADHD symptom severity. SNPs within angiogenic (NRP1 & NRP2), neurotrophic (NTRK1 & NTRK3), cytokine (IL16 & S100B), and kynurenine (CCBL1 & CCBL2) genes moderate the association between birth weight centile and ADHDsymptom severity. The SNPmain effects and SNP?birth weight centile interactions remained significant after adjusting
for multiple testing. Genetic variability in angiogenic, neurotrophic, and inflammatory systems may moderate the association between restricted prenatal growth, a proxy for an adverse prenatal environment, and risk to develop ADHD.

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8.Etl.and.E.Sonuga-Barke_Angiogenic, Neurotrophic,andInflammatorySystem.pdf - Accepted Manuscript
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Accepted/In Press date: 25 September 2014
e-pub ahead of print date: 25 October 2014
Published date: December 2014
Keywords: attention deficit hyperactivity disorder, birthweight, gene-environment interaction, neurotrophin, developmental origins of health and disease
Organisations: Psychology

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Local EPrints ID: 373950
URI: http://eprints.soton.ac.uk/id/eprint/373950
ISSN: 1552-4841
PURE UUID: cb6c2921-dd67-4a3b-b0a8-95573767801b

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Date deposited: 03 Feb 2015 14:44
Last modified: 14 Mar 2024 18:59

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Contributors

Author: Taylor F. Smith
Author: Arthur D. Anastopoulos
Author: Melanie E. Garrett
Author: Alejandro Arias-Vasquez
Author: Barbara Franke
Author: Robert D. Oades
Author: Edmund J.S. Sonuga-Barke
Author: Philip Asherson
Author: Michael Gill
Author: Jan K. Buitelaar
Author: Joseph A. Sergeant
Author: Scott H. Kollins
Author: Stephen V. Faraone
Author: Allison Ashley-Koch

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