Evidence map›Paper›PMID 25600112›Full record

ReviewMolecular psychiatry2015

The molecular genetic architecture of attention deficit hyperactivity disorder.

Z Hawi, T D R Cummins, J Tong, B Johnson, R Lau, W Samarrai, M A Bellgrove

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 5 pooled it
21.9field-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

100 citing papers in PubMed, 5 syntheses or guidelines pooled it, 214 citations in OpenAlex.

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40 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

7 authors at 2 institutions in 2 countries.

Z HawiSchool of Psychological Sciences, Monash University, Melbourne, VIC, Australia.
T D R CumminsSchool of Psychological Sciences, Monash University, Melbourne, VIC, Australia.
J TongSchool of Psychological Sciences, Monash University, Melbourne, VIC, Australia.
B JohnsonSchool of Psychological Sciences, Monash University, Melbourne, VIC, Australia.
R LauSchool of Psychological Sciences, Monash University, Melbourne, VIC, Australia.
W SamarraiNew York City College of Technology, City University of New York, New York, NY, USA.
M A BellgroveSchool of Psychological Sciences, Monash University, Melbourne, VIC, Australia.
Monash University · AUCity University of New York · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Attention deficit hyperactivity disorder (ADHD) is a common childhood behavioral condition which affects 2-10% of school age children worldwide. Although the underlying molecular mechanism for the disorder is poorly understood, familial, twin and adoption studies suggest a strong genetic component. Here we provide a state-of-the-art review of the molecular genetics of ADHD incorporating evidence from candidate gene and linkage designs, as well as genome-wide association (GWA) studies of common single-nucleotide polymorphisms (SNPs) and rare copy number variations (CNVs). Bioinformatic methods such as functional enrichment analysis and protein-protein network analysis are used to highlight biological processes of likely relevance to the aetiology of ADHD. Candidate gene associations of minor effect size have been replicated across a number of genes including SLC6A3, DRD5, DRD4, SLC6A4, LPHN3, SNAP-25, HTR1B, NOS1 and GIT1. Although case-control SNP-GWAS have had limited success in identifying common genetic variants for ADHD that surpass critical significance thresholds, quantitative trait designs suggest promising associations with Cadherin13 and glucose-fructose oxidoreductase domain 1 genes. Further, CNVs mapped to glutamate receptor genes (GRM1, GRM5, GRM7 and GRM8) have been implicated in the aetiology of the disorder and overlap with bioinformatic predictions based on ADHD GWAS SNP data regarding enriched pathways. Although increases in sample size across multi-center cohorts will likely yield important new results, we advocate that this must occur in parallel with a shift away from categorical case-control approaches that view ADHD as a unitary construct, towards dimensional approaches that incorporate endophenotypes and statistical classification methods.

Indexed as

Attention Deficit Disorder with HyperactivityDNA Copy Number VariationsGenetic Predisposition to DiseaseGenome-Wide Association StudyHumans

Identifiers

PMID25600112
OpenAlexW1973331389

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.