Evidence map›Paper›PMID 15322957›Full record

ArticleEuropean child & adolescent psychiatry2004

Attention-Deficit Hyperactivity Disorder in the post-genomic era.

Philip Asherson, IMAGE Consortium

Abstract read
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In one paragraph

Article in European child & adolescent psychiatry, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

40 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Meta-analysis of genome-wide linkage scans of attention deficit hyperactivity disorder.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2008
    Pooled it
  3. Functional MRI in ADHD: a systematic literature review.Expert review of neurotherapeutics · 2007
    Pooled it
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  12. The role of sleep problems and circadian clock genes in childhood psychiatric disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2012
    Review
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  15. Polymorphisms of the steroid sulfatase (STS) gene are associated with attention deficit hyperactivity disorder and influence brain tissue mRNA expression.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2010
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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

2 authors.

Philip AshersonMRC Social Genetic Developmental, Psychiatry Research Centre, Institute of Psychiatry, Kings College London, de Crespigny Park, London SE5 8AF, UK. p.asherson@iop.kcl.ac.uk
IMAGE Consortium

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundADHD is a common and complex genetic disorder. Genetic risk factors are expected to be multiple, have small effect sizes when considered individually and to interact with each other and with environmental factors.

objectiveTo describe the difficulties involved in the genetic investigation of such a complex disorder and give a prospective for the future.

methodsReview based on empirical literature and project description.

resultsConsiderable progress has been achieved through the association analysis of candidate gene loci. Linkage scans using affected sibling pairs have identified a number of potential loci that may lead to the identification of novel genes of moderate effect size. Quantitative trait locus (QTL) approaches provide powerful complementary strategies that have the potential to link the categorical disorder to continuously distributed traits associated more closely with underlying genetic liability in the general population. Success in identifying some associated genes has been complemented by functional studies that seek to understand the mode of action of such genes.

conclusionProgress in understanding the mechanisms involved has not been straightforward and many inconsistencies have arisen. In order to take advantage of the potential for progress that stems from the genetic findings it will be important to draw upon a variety of approaches and experimental paradigms. A functional genomic approach to ADHD means that investigation of gene function is carried out at various levels of analysis, not only at the level of molecular and cellular function but also at the level of psychological processes, neuronal networks, environmental interactions and behavioural outcomes.

Indexed as

Attention Deficit Disorder with HyperactivityChildDopamine Plasma Membrane Transport ProteinsGenetic LinkageGenomicsHumansMembrane GlycoproteinsMembrane ProteinsMembrane Transport ProteinsNerve Tissue ProteinsPhenotypeReceptors, Dopamine D1Receptors, Dopamine D2Receptors, Dopamine D4Receptors, Dopamine D5SerotoninDopamine Plasma Membrane Transport ProteinsDRD4 protein, humanDRD5 protein, humanMembrane GlycoproteinsMembrane ProteinsMembrane Transport ProteinsNerve Tissue ProteinsReceptors, Dopamine D1Receptors, Dopamine D2Receptors, Dopamine D4Receptors, Dopamine D5SerotoninSNAP25 protein, humanSynaptosomal-Associated Protein 25

Identifiers

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Registered trials

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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.