Evidence map›Paper›PMID 19506906›Full record

SynthesisHuman genetics2009

Candidate gene studies of ADHD: a meta-analytic review.

Ian R Gizer, Courtney Ficks, Irwin D Waldman

Abstract readMeta-AnalysisReview
PubMed Publisher
In one paragraph

Synthesis in Human genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 399 papers, 12 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
399citing papers in PubMed, 12 pooled it
40.4field-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

399 citing papers in PubMed, 12 syntheses or guidelines pooled it, 1,005 citations in OpenAlex.

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  13. Trial
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  16. Anoctamin 2 deletion alters dopamine-related signaling and impairs inhibitory behavioral control in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  17. Article
  18. Effects of NR3C1 and COMT Genes on Attention-Deficit/Hyperactivity Disorder and Accompanying Aggressiveness: A Cross-Sectional Study in a Clinical Sample.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2026
    Article
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339 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Ian R GizerDepartment of Genetics, University of North Carolina at Chapel Hill, 120 Mason Farm Road, Room 5015 Genetic Medicine Building CB 7264, Chapel Hill, NC 27599-7264, USA. igizer@unc.edu
Courtney Ficks
Irwin D Waldman
Emory University · USUniversity of North Carolina at Chapel Hill · US

Funding

Supplement to Molecular and Cellular Studies on Alcohol's ActionsT32AA007573 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FULTON T CREWS, Thomas L. Kash · 1997 to 2026
$9.3M
COLLABORATIVE ADHD GENETICS CONFERENCER13MH059126 · NIMH · UPSTATE MEDICAL UNIVERSITY · PI FARAONE, STEPHEN V · 1999 to 2014
$957k
NIAAA NIH HHS T32 AA007573NIMH NIH HHS R13MH59126-0641
6 · The paper itself

Abstract

Quantitative genetic studies (i.e., twin and adoption studies) suggest that genetic influences contribute substantially to the development of attention deficit hyperactivity disorder (ADHD). Over the past 15 years, considerable efforts have been made to identify genes involved in the etiology of this disorder resulting in a large and often conflicting literature of candidate gene associations for ADHD. The first aim of the present study was to conduct a comprehensive meta-analytic review of this literature to determine which candidate genes show consistent evidence of association with childhood ADHD across studies. The second aim was to test for heterogeneity across studies in the effect sizes for each candidate gene as its presence might suggest moderating variables that could explain inconsistent results. Significant associations were identified for several candidate genes including DAT1, DRD4, DRD5, 5HTT, HTR1B, and SNAP25. Further, significant heterogeneity was observed for the associations between ADHD and DAT1, DRD4, DRD5, DBH, ADRA2A, 5HTT, TPH2, MAOA, and SNAP25, suggesting that future studies should explore potential moderators of these associations (e.g., ADHD subtype diagnoses, gender, exposure to environmental risk factors). We conclude with a discussion of these findings in relation to emerging themes relevant to future studies of the genetics of ADHD.

Indexed as

AllelesAttention Deficit Disorder with HyperactivityCase-Control StudiesChildDopamine beta-HydroxylaseDopamine Plasma Membrane Transport ProteinsGenetic MarkersHumansMonoamine OxidasePolymorphism, GeneticReceptors, Adrenergic, alpha-2Receptors, Dopamine D4Receptors, Dopamine D5Receptor, Serotonin, 5-HT1BReceptor, Serotonin, 5-HT2ASynaptosomal-Associated Protein 25ADRA2A protein, humanDopamine beta-HydroxylaseDopamine Plasma Membrane Transport ProteinsGenetic MarkersMonoamine OxidaseReceptors, Adrenergic, alpha-2Receptors, Dopamine D4Receptors, Dopamine D5Receptor, Serotonin, 5-HT1BReceptor, Serotonin, 5-HT2ASLC6A3 protein, humanSNAP25 protein, humanSynaptosomal-Associated Protein 25TPH2 protein, humanTryptophan Hydroxylase

Identifiers

PMID19506906
OpenAlexW2086710797

What OpenQuestion holds

Textmetadata
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.