No genetic association between attention-deficit/hyperactivity disorder (ADHD) and Parkinson’s disease in nine ADHD candidate SNPs

International Parkinson Disease Genomics Consortium members

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Attention-deficit/hyperactivity disorder (ADHD) and Parkinson’s disease (PD) involve pathological changes in brain structures such as the basal ganglia, which are essential for the control of motor and cognitive behavior and impulsivity. The cause of ADHD and PD remains unknown, but there is increasing evidence that both seem to result from a complicated interplay of genetic and environmental factors affecting numerous cellular processes and brain regions. To explore the possibility of common genetic pathways within the respective pathophysiologies, nine ADHD candidate single nucleotide polymorphisms (SNPs) in seven genes were tested for association with PD in 5333 cases and 12,019 healthy controls: one variant, respectively, in the genes coding for synaptosomal-associated protein 25k (SNAP25), the dopamine (DA) transporter (SLC6A3; DAT1), DA receptor D4 (DRD4), serotonin receptor 1B (HTR1B), tryptophan hydroxylase 2 (TPH2), the norepinephrine transporter SLC6A2 and three SNPs in cadherin 13 (CDH13). Information was extracted from a recent meta-analysis of five genome-wide association studies, in which 7,689,524 SNPs in European samples were successfully imputed. No significant association was observed after correction for multiple testing. Therefore, it is reasonable to conclude that candidate variants implicated in the pathogenesis of ADHD do not play a substantial role in PD.

Original languageEnglish
Pages (from-to)121-127
Number of pages7
JournalADHD Attention Deficit and Hyperactivity Disorders
Volume9
Issue number2
DOIs
Publication statusPublished - 1 Jun 2017

Fingerprint

Attention Deficit Disorder with Hyperactivity
Single Nucleotide Polymorphism
Parkinson Disease
Norepinephrine Plasma Membrane Transport Proteins
Receptor, Serotonin, 5-HT1B
Tryptophan Hydroxylase
Dopamine Plasma Membrane Transport Proteins
Impulsive Behavior
Genome-Wide Association Study
Dopamine Receptors
Brain
Basal Ganglia
Genes
Meta-Analysis

Keywords

  • ADHD
  • CDH13
  • Dopamine transporter
  • GWAS
  • Parkinson’s disease
  • SNPs

ASJC Scopus subject areas

  • Clinical Psychology
  • Psychiatry and Mental health

Cite this

No genetic association between attention-deficit/hyperactivity disorder (ADHD) and Parkinson’s disease in nine ADHD candidate SNPs. / International Parkinson Disease Genomics Consortium members.

In: ADHD Attention Deficit and Hyperactivity Disorders, Vol. 9, No. 2, 01.06.2017, p. 121-127.

Research output: Contribution to journalArticle

@article{de584cfa33a04b00a3612dd435909691,
title = "No genetic association between attention-deficit/hyperactivity disorder (ADHD) and Parkinson’s disease in nine ADHD candidate SNPs",
abstract = "Attention-deficit/hyperactivity disorder (ADHD) and Parkinson’s disease (PD) involve pathological changes in brain structures such as the basal ganglia, which are essential for the control of motor and cognitive behavior and impulsivity. The cause of ADHD and PD remains unknown, but there is increasing evidence that both seem to result from a complicated interplay of genetic and environmental factors affecting numerous cellular processes and brain regions. To explore the possibility of common genetic pathways within the respective pathophysiologies, nine ADHD candidate single nucleotide polymorphisms (SNPs) in seven genes were tested for association with PD in 5333 cases and 12,019 healthy controls: one variant, respectively, in the genes coding for synaptosomal-associated protein 25k (SNAP25), the dopamine (DA) transporter (SLC6A3; DAT1), DA receptor D4 (DRD4), serotonin receptor 1B (HTR1B), tryptophan hydroxylase 2 (TPH2), the norepinephrine transporter SLC6A2 and three SNPs in cadherin 13 (CDH13). Information was extracted from a recent meta-analysis of five genome-wide association studies, in which 7,689,524 SNPs in European samples were successfully imputed. No significant association was observed after correction for multiple testing. Therefore, it is reasonable to conclude that candidate variants implicated in the pathogenesis of ADHD do not play a substantial role in PD.",
keywords = "ADHD, CDH13, Dopamine transporter, GWAS, Parkinson’s disease, SNPs",
author = "{International Parkinson Disease Genomics Consortium members} and Geissler, {Julia M.} and Mike Nalls and Vincent Plagnol and Hernandez, {Dena G.} and Manu Sharma and Sheerin, {Una Marie} and Mohamad Saad and Mohamad Saad and Claudia Schulte and Suzanne Lesage and Sigurlaug Sveinbj{\"o}rnsd{\'o}ttir and Sampath Arepalli and Roger Barker and Yoav Ben-Shlomo and Berendse, {Henk W.} and Daniela Berg and Kailash Bhatia and deBie, {Rob M.A.} and Alessandro Biffi and Bas Bloem and Zoltan Bochdanovits and Michael Bonin and Bras, {Jose M.} and Kathrin Brockmann and Janet Brooks and Burn, {David J.} and Gavin Charlesworth and Honglei Chen and Chinnery, {Patrick F.} and Sean Chong and Clarke, {Carl E.} and Cookson, {Mark R.} and Cooper, {J. Mark} and Corvol, {Jean Christophe} and Carl Counsell and Philippe Damier and Dartigues, {Jean Fran{\cc}ois} and Panos Deloukas and G{\"u}nther Deuschl and Dexter, {David T.} and vanDijk, {Karin D.} and Allissa Dillman and Frank Durif and Alexandra D{\"u}rr and Sarah Edkins and Evans, {Jonathan R.} and Thomas Foltynie and Jianjun Gao and Michelle Gardner and Gibbs, {J. Raphael}",
year = "2017",
month = "6",
day = "1",
doi = "10.1007/s12402-017-0219-8",
language = "English",
volume = "9",
pages = "121--127",
journal = "ADHD Attention Deficit and Hyperactivity Disorders",
issn = "1866-6116",
publisher = "Springer Wien",
number = "2",

}

TY - JOUR

T1 - No genetic association between attention-deficit/hyperactivity disorder (ADHD) and Parkinson’s disease in nine ADHD candidate SNPs

AU - International Parkinson Disease Genomics Consortium members

AU - Geissler, Julia M.

AU - Nalls, Mike

AU - Plagnol, Vincent

AU - Hernandez, Dena G.

AU - Sharma, Manu

AU - Sheerin, Una Marie

AU - Saad, Mohamad

AU - Saad, Mohamad

AU - Schulte, Claudia

AU - Lesage, Suzanne

AU - Sveinbjörnsdóttir, Sigurlaug

AU - Arepalli, Sampath

AU - Barker, Roger

AU - Ben-Shlomo, Yoav

AU - Berendse, Henk W.

AU - Berg, Daniela

AU - Bhatia, Kailash

AU - deBie, Rob M.A.

AU - Biffi, Alessandro

AU - Bloem, Bas

AU - Bochdanovits, Zoltan

AU - Bonin, Michael

AU - Bras, Jose M.

AU - Brockmann, Kathrin

AU - Brooks, Janet

AU - Burn, David J.

AU - Charlesworth, Gavin

AU - Chen, Honglei

AU - Chinnery, Patrick F.

AU - Chong, Sean

AU - Clarke, Carl E.

AU - Cookson, Mark R.

AU - Cooper, J. Mark

AU - Corvol, Jean Christophe

AU - Counsell, Carl

AU - Damier, Philippe

AU - Dartigues, Jean François

AU - Deloukas, Panos

AU - Deuschl, Günther

AU - Dexter, David T.

AU - vanDijk, Karin D.

AU - Dillman, Allissa

AU - Durif, Frank

AU - Dürr, Alexandra

AU - Edkins, Sarah

AU - Evans, Jonathan R.

AU - Foltynie, Thomas

AU - Gao, Jianjun

AU - Gardner, Michelle

AU - Gibbs, J. Raphael

PY - 2017/6/1

Y1 - 2017/6/1

N2 - Attention-deficit/hyperactivity disorder (ADHD) and Parkinson’s disease (PD) involve pathological changes in brain structures such as the basal ganglia, which are essential for the control of motor and cognitive behavior and impulsivity. The cause of ADHD and PD remains unknown, but there is increasing evidence that both seem to result from a complicated interplay of genetic and environmental factors affecting numerous cellular processes and brain regions. To explore the possibility of common genetic pathways within the respective pathophysiologies, nine ADHD candidate single nucleotide polymorphisms (SNPs) in seven genes were tested for association with PD in 5333 cases and 12,019 healthy controls: one variant, respectively, in the genes coding for synaptosomal-associated protein 25k (SNAP25), the dopamine (DA) transporter (SLC6A3; DAT1), DA receptor D4 (DRD4), serotonin receptor 1B (HTR1B), tryptophan hydroxylase 2 (TPH2), the norepinephrine transporter SLC6A2 and three SNPs in cadherin 13 (CDH13). Information was extracted from a recent meta-analysis of five genome-wide association studies, in which 7,689,524 SNPs in European samples were successfully imputed. No significant association was observed after correction for multiple testing. Therefore, it is reasonable to conclude that candidate variants implicated in the pathogenesis of ADHD do not play a substantial role in PD.

AB - Attention-deficit/hyperactivity disorder (ADHD) and Parkinson’s disease (PD) involve pathological changes in brain structures such as the basal ganglia, which are essential for the control of motor and cognitive behavior and impulsivity. The cause of ADHD and PD remains unknown, but there is increasing evidence that both seem to result from a complicated interplay of genetic and environmental factors affecting numerous cellular processes and brain regions. To explore the possibility of common genetic pathways within the respective pathophysiologies, nine ADHD candidate single nucleotide polymorphisms (SNPs) in seven genes were tested for association with PD in 5333 cases and 12,019 healthy controls: one variant, respectively, in the genes coding for synaptosomal-associated protein 25k (SNAP25), the dopamine (DA) transporter (SLC6A3; DAT1), DA receptor D4 (DRD4), serotonin receptor 1B (HTR1B), tryptophan hydroxylase 2 (TPH2), the norepinephrine transporter SLC6A2 and three SNPs in cadherin 13 (CDH13). Information was extracted from a recent meta-analysis of five genome-wide association studies, in which 7,689,524 SNPs in European samples were successfully imputed. No significant association was observed after correction for multiple testing. Therefore, it is reasonable to conclude that candidate variants implicated in the pathogenesis of ADHD do not play a substantial role in PD.

KW - ADHD

KW - CDH13

KW - Dopamine transporter

KW - GWAS

KW - Parkinson’s disease

KW - SNPs

UR - http://www.scopus.com/inward/record.url?scp=85011887445&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85011887445&partnerID=8YFLogxK

U2 - 10.1007/s12402-017-0219-8

DO - 10.1007/s12402-017-0219-8

M3 - Article

VL - 9

SP - 121

EP - 127

JO - ADHD Attention Deficit and Hyperactivity Disorders

JF - ADHD Attention Deficit and Hyperactivity Disorders

SN - 1866-6116

IS - 2

ER -