Evidence map›Paper›PMID 22105624›Full record

ReviewMolecular psychiatry2012

The genetics of attention deficit/hyperactivity disorder in adults, a review.

B Franke, S V Faraone, P Asherson, J Buitelaar, C H D Bau, J A Ramos-Quiroga, E Mick, E H Grevet, S Johansson, J Haavik and 4 more

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Molecular psychiatry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers, 11 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed, 11 pooled it
16.4field-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

162 citing papers in PubMed, 11 syntheses or guidelines pooled it, 431 citations in OpenAlex.

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  11. Meta-analysis of increased heart rate and blood pressure associated with CNS stimulant treatment of ADHD in adults.European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2013
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102 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

14 authors at 11 institutions in 7 countries.

B FrankeDepartment of Human Genetics, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. b.franke@antrg.umcn.nl
S V Faraone
P Asherson
J Buitelaar
C H D Bau
J A Ramos-Quiroga
E Mick
E H Grevet
S Johansson
J Haavik
K-P Lesch
B Cormand
A Reif
International Multicentre persistent ADHD CollaboraTion
Haukeland University Hospital · NORadboud University Nijmegen · NLHospital de Clínicas de Porto Alegre · BRInstitut de Biomedicina de la Universitat de BarcelonaKing's College London · GBMaastricht University · NLSUNY Upstate Medical University · USUniversidade Federal do Rio Grande do Sul · BRUniversity of Massachusetts Chan Medical School · USUniversity of Würzburg · DEVall d'Hebron Hospital Universitari · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The adult form of attention deficit/hyperactivity disorder (aADHD) has a prevalence of up to 5% and is the most severe long-term outcome of this common neurodevelopmental disorder. Family studies in clinical samples suggest an increased familial liability for aADHD compared with childhood ADHD (cADHD), whereas twin studies based on self-rated symptoms in adult population samples show moderate heritability estimates of 30-40%. However, using multiple sources of information, the heritability of clinically diagnosed aADHD and cADHD is very similar. Results of candidate gene as well as genome-wide molecular genetic studies in aADHD samples implicate some of the same genes involved in ADHD in children, although in some cases different alleles and different genes may be responsible for adult versus childhood ADHD. Linkage studies have been successful in identifying loci for aADHD and led to the identification of LPHN3 and CDH13 as novel genes associated with ADHD across the lifespan. In addition, studies of rare genetic variants have identified probable causative mutations for aADHD. Use of endophenotypes based on neuropsychology and neuroimaging, as well as next-generation genome analysis and improved statistical and bioinformatic analysis methods hold the promise of identifying additional genetic variants involved in disease etiology. Large, international collaborations have paved the way for well-powered studies. Progress in identifying aADHD risk genes may provide us with tools for the prediction of disease progression in the clinic and better treatment, and ultimately may help to prevent persistence of ADHD into adulthood.

Indexed as

GeneticsAdultAttention Deficit Disorder with HyperactivityCadherinsFamily HealthGenetic Association StudiesGenetic LinkageGenetic Predisposition to DiseaseHumansNeuroimagingReceptors, G-Protein-CoupledReceptors, PeptideADGRL3 protein, humanCadherinsH-cadherinReceptors, G-Protein-CoupledReceptors, Peptide

Identifiers

PMID22105624
PMCPMC3449233
OpenAlexW2125832432

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.