Evidence map›Paper›PMID 25875332›Full record

SynthesisPloS one2015

Genome-wide analysis of attention deficit hyperactivity disorder in Norway.

Tetyana Zayats, Lavinia Athanasiu, Ida Sonderby, Srdjan Djurovic, Lars T Westlye, Christian K Tamnes, Tormod Fladby, Heidi Aase, Pål Zeiner, Ted Reichborn-Kjennerud and 5 more

Open access · goldAbstract readMeta-Analysis
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 3 pooled it
8.6field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed, 3 syntheses or guidelines pooled it, 85 citations in OpenAlex.

  1. Shared genetic background between children and adults with attention deficit/hyperactivity disorder.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020
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  13. Decreased Brain pH and Pathophysiology in Schizophrenia.International journal of molecular sciences · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 6 institutions in 1 country.

Tetyana ZayatsK.G. Jebsen Centre for Neuropsychiatric Disorders, Department of Biomedicine, University of Bergen, Bergen, Norway.
Lavinia AthanasiuNORMENT, K.G. Jebsen Centre for Psychosis Research, Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Ida SonderbyNORMENT, K.G. Jebsen Centre for Psychosis Research, Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Srdjan DjurovicDepartment of Medical Genetics, Oslo University Hospital, Oslo, Norway; NORMENT, K.G. Jebsen Centre for Psychosis Research, Department of Clinical Science, University of Bergen, Bergen, Norway.
Lars T WestlyeNORMENT, K.G. Jebsen Centre for Psychosis Research, Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Psychology, University of Oslo, Oslo, Norway.
Christian K TamnesResearch Group for Lifespan Changes in Brain and Cognition, Department of Psychology, University Of Oslo, Oslo, Norway.
Tormod FladbyDepartment of Neurology, Akershus University Hospital, Lørenskog, Norway; University of Oslo, Institute of Clinical Medicine, Oslo, Norway.
Heidi AaseDivision of Mental Health, Norwegian Institute of Public Health, Oslo, Norway.
Pål ZeinerOslo University Hospital, Child and Adolescent Mental Health Research Unit, Oslo, Norway.
Ted Reichborn-KjennerudDivision of Mental Health, Norwegian Institute of Public Health, Oslo, Norway; University of Oslo, Institute of Clinical Medicine, Oslo, Norway.
Per M KnappskogK.G. Jebsen Centre for Neuropsychiatric Disorders, Department of Clinical Science, University of Bergen, Bergen, Norway; Center for Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen, Norway.
Gun Peggy KnudsenDivision of Mental Health, Norwegian Institute of Public Health, Oslo, Norway.
Ole A AndreassenNORMENT, K.G. Jebsen Centre for Psychosis Research, Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Stefan JohanssonK.G. Jebsen Centre for Neuropsychiatric Disorders, Department of Clinical Science, University of Bergen, Bergen, Norway; Center for Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen, Norway.
Jan HaavikK.G. Jebsen Centre for Neuropsychiatric Disorders, Department of Biomedicine, University of Bergen, Bergen, Norway; Division of Psychiatry, Haukeland University Hospital, Bergen, Norway.
University of Bergen · NOUniversity of Oslo · NOOslo University Hospital · NONorwegian Institute of Public Health · NOAkershus University Hospital · NOHaukeland University Hospital · NO

Funding

Gene-Environment Interactions in an Autism Birth CohortU01NS047537 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LIPKIN, W. IAN · 2003 to 2013
$27.0M
NIEHS NIH HHS N01 ES075558NIEHS NIH HHS N0-ES-75558NINDS NIH HHS 1 U01 NS 047537-01NINDS NIH HHS U01 NS047537
6 · The paper itself

Abstract

backgroundAttention deficit hyperactivity disorder (ADHD) is a highly heritable neuropsychiatric condition, but it has been difficult to identify genes underlying this disorder. This study aimed to explore genetics of ADHD in an ethnically homogeneous Norwegian population by means of a genome-wide association (GWA) analysis followed by examination of candidate loci. MATERIALS AND

methodsParticipants were recruited through Norwegian medical and birth registries as well as the general population. Presence of ADHD was defined according to DSM-IV criteria. Genotyping was performed using Illumina Human OmniExpress-12v1 microarrays. Statistical analyses were divided into several steps: (1) genome-wide association in the form of logistic regression in PLINK and follow-up pathway analyses performed in DAPPLE and INRICH softwares, (2) SNP-heritability calculated using genome-wide complex trait analysis (GCTA) tool, (3) gene-based association tests carried out in JAG software, and (4) evaluation of previously reported genome-wide signals and candidate genes of ADHD.

resultsIn total, 1.358 individuals (478 cases and 880 controls) and 598.384 autosomal SNPs were subjected to GWA analysis. No single polymorphism reached genome-wide significance. The strongest signal was observed at rs9949006 in the ENSG00000263745 gene (OR=1.51, 95% CI 1.28-1.79, p=1.38E-06). Pathway analyses of the top SNPs implicated genes involved in the regulation of gene expression, cell adhesion and inflammation. Among previously identified ADHD candidate genes, prominent association signals were observed for SLC9A9 (rs1393072, OR=1.46, 95% CI = 1.21-1.77, p=9.95E-05) and TPH2 (rs17110690, OR = 1.38, 95% CI = 1.14-1.66, p=8.31E-04).

conclusionThis study confirms the complexity and heterogeneity of ADHD etiology. Taken together with previous findings, our results point to a spectrum of biological mechanisms underlying the symptoms of ADHD, providing targets for further genetic exploration of this complex disorder.

Indexed as

Genetic Predisposition to DiseaseGenome-Wide Association StudyAttention Deficit Disorder with HyperactivityGenotypeHumansPhenotypePolymorphism, Single NucleotideSodium-Hydrogen ExchangersTryptophan HydroxylaseSLC9A9 protein, humanSodium-Hydrogen ExchangersTPH2 protein, humanTryptophan Hydroxylase

Identifiers

PMID25875332
PMCPMC4395400
OpenAlexW2095280681

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.