Evidence map›Paper›PMID 30935427›Full record

ArticlePsychological medicine2020

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Esther D A van Duin, Jenny Ceccarini, Jan Booij, Zuzana Kasanova, Claudia Vingerhoets, Jytte van Huijstee, Alexander Heinzel, Siamak Mohammadkhani-Shali, Oliver Winz, Felix Mottaghy and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Psychological medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 48% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
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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

12 authors at 5 institutions in 4 countries.

Esther D A van DuinDepartment of Psychiatry & Neuropsychology, Maastricht University, Maastricht, The Netherlands.ORCID 0000-0002-4679-522X
Jenny CeccariniDepartment of Nuclear Medicine and Molecular Imaging, Division of Imaging and Pathology, University Hospital Leuven, KU Leuven, Belgium.
Jan BooijAcademic Medical Center, Amsterdam, The Netherlands.
Zuzana KasanovaDepartment of Neuroscience, Center for Contextual Psychiatry, KU Leuven - Leuven University, Leuven, Belgium.
Claudia VingerhoetsDepartment of Psychiatry & Neuropsychology, Maastricht University, Maastricht, The Netherlands.
Jytte van HuijsteeDepartment of Psychiatry & Neuropsychology, Maastricht University, Maastricht, The Netherlands.
Alexander HeinzelDepartment of Nuclear Medicine, University Hospital RWTH, Aachen University, Aachen, Germany.
Siamak Mohammadkhani-ShaliDepartment of Nuclear Medicine, University Hospital RWTH, Aachen University, Aachen, Germany.
Oliver WinzDepartment of Nuclear Medicine, University Hospital RWTH, Aachen University, Aachen, Germany.
Felix MottaghyDepartment of Nuclear Medicine, University Hospital RWTH, Aachen University, Aachen, Germany.
Inez Myin-GermeysDepartment of Neuroscience, Center for Contextual Psychiatry, KU Leuven - Leuven University, Leuven, Belgium.
Thérèse van AmelsvoortDepartment of Psychiatry & Neuropsychology, Maastricht University, Maastricht, The Netherlands.
KU Leuven · BEMaastricht University · NLRWTH Aachen University · DEAmsterdam UMC Location University of Amsterdam · NLUniversity Medical Center · US

Funding

"4/5 International Consortium on Brain and Behavior in 22q11.2 Deletion Syndrome"U01MH101722 · NIMH · KATHOLIEKE UNIVERSITEIT LEUVEN · PI SWILLEN, ANN · 2013 to 2016
$1.3M
NIMH NIH HHS U01 MH101722
6 · The paper itself

Abstract

backgroundThe 22q11.2 deletion syndrome (22q11DS) is caused by a deletion on chromosome 22 locus q11.2. This copy number variant results in haplo-insufficiency of the catechol-O-methyltransferase (COMT) gene, and is associated with a significant increase in the risk for developing cognitive impairments and psychosis. The COMT gene encodes an enzyme that primarily modulates clearance of dopamine (DA) from the synaptic cleft, especially in the prefrontal cortical areas. Consequently, extracellular DA levels may be increased in prefrontal brain areas in 22q11DS, which may underlie the well-documented susceptibility for cognitive impairments and psychosis in affected individuals. This study aims to examine DA D2/3 receptor binding in frontal brain regions in adults with 22q11DS, as a proxy of frontal DA levels.

methodsThe study was performed in 14 non-psychotic, relatively high functioning adults with 22q11DS and 16 age- and gender-matched healthy controls (HCs), who underwent DA D2/3 receptor [18F]fallypride PET imaging. Frontal binding potential (BPND) was used as the main outcome measure.

resultsBPND was significantly lower in adults with 22q11DS compared with HCs in the prefrontal cortex and the anterior cingulate gyrus. After Bonferroni correction significance remained for the anterior cingulate gyrus. There were no between-group differences in BPND in the orbitofrontal cortex and anterior cingulate cortex.

conclusionsThis study is the first to demonstrate lower frontal D2/3 receptor binding in adults with 22q11DS. It suggests that a 22q11.2 deletion affects frontal dopaminergic neurotransmission.

Indexed as

Positron-Emission TomographyAdultBenzamidesBrain MappingCatechol O-MethyltransferaseDiGeorge SyndromeFemaleHumansMaleMiddle AgedPrefrontal CortexPsychotic DisordersReceptors, Dopamine D2Young AdultBenzamidesCatechol O-MethyltransferaseDRD2 protein, humanfallyprideReceptors, Dopamine D2[18F]fallypride22q11DSCOMTdopaminefrontalPET

Identifiers

PMID30935427
PMCPMC7168654
OpenAlexW2929505304

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.