Evidence map›Paper›PMID 32448020›Full record

Trial reportJournal of psychopharmacology (Oxford, England)2020

Glutamatergic and GABAergic reactivity and cognition in 22q11.2 deletion syndrome and healthy volunteers: A randomized double-blind 7-Tesla pharmacological MRS study.

Claudia Vingerhoets, Desmond Hy Tse, Mathilde van Oudenaren, Dennis Hernaus, Esther van Duin, Janneke Zinkstok, Johannes G Ramaekers, Jacobus Fa Jansen, Grainne McAlonan, Therese van Amelsvoort

Open access · hybridAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Journal of psychopharmacology (Oxford, England), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 2 pooled it
1.2field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 2 syntheses or guidelines pooled it, 18 citations in OpenAlex.

  1. Pooled it
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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

10 authors at 3 institutions in 2 countries.

Claudia VingerhoetsDepartment of Psychiatry & Neuropsychology, Maastricht University, Maastricht, the Netherlands.ORCID 0000-0001-7790-5041
Desmond Hy TseFaculty of Psychology and Neuroscience, Maastricht University, Maastricht, the Netherlands.
Mathilde van OudenarenDepartment of Psychiatry & Neuropsychology, Maastricht University, Maastricht, the Netherlands.
Dennis HernausDepartment of Psychiatry & Neuropsychology, Maastricht University, Maastricht, the Netherlands.
Esther van DuinDepartment of Psychiatry & Neuropsychology, Maastricht University, Maastricht, the Netherlands.
Janneke ZinkstokDepartment of Psychiatry & UMC Utrecht Brain Center, University Medical Center, Utrecht, the Netherlands.
Johannes G RamaekersFaculty of Psychology and Neuroscience, Maastricht University, Maastricht, the Netherlands.
Jacobus Fa JansenDepartment of Radiology, Maastricht University Medical Center, Maastricht University, Maastricht, the Netherlands.
Grainne McAlonanThe Sackler Institute for Translational Neurodevelopment, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Therese van AmelsvoortDepartment of Psychiatry & Neuropsychology, Maastricht University, Maastricht, the Netherlands.
Maastricht University · NLKing's College London · GBUniversity Medical Center Utrecht · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims22q11.2 deletion syndrome (22q11.2DS) is associated with impaired cognitive functioning. Glutamatergic pathways have been linked with cognition and are hypothesized to be disrupted in 22q11.2DS patients, possibly 'shifting' the excitatory (glutamate)/inhibitory (GABA) balance. Hence, the glutamate/GABA balance may constitute a target for pharmacological treatment. We aimed to examine alterations of glutamate/GABA metabolites in 22q11.2DS

methodsSeventeen 22q11.2DS patients and 20 matched healthy controls were enrolled in this randomized double-blind placebo-controlled crossover study. Glutamate and glutamine concentrations in the anterior cingulate cortex (ACC) and striatum, as well as ACC GABA concentrations were obtained after placebo and after a single dose of 50 mg riluzole using 7-Tesla magnetic resonance spectroscopy (MRS). Within the 22q11.2DS group, the relationship between metabolite concentrations and cognition was examined.

resultsNo group differences were found in ACC and striatal metabolite concentrations following placebo. Riluzole numerically decreased ACC ( DISCUSSION: We did not demonstrate altered ACC and striatal metabolite concentrations in 22q11.2DS. Nevertheless, these results suggest that glutamate and GABA can be modulated with a single dose of riluzole. Possibly, riluzole may have memory-enhancing effects in 22q11.2DS. Future studies should examine the long-term effects of riluzole on cognition.

Indexed as

AdultAttentionCognitionCorpus StriatumCross-Over StudiesDiGeorge SyndromeDouble-Blind MethodExcitatory Amino Acid AntagonistsFemalegamma-Aminobutyric AcidGlutamic AcidGyrus CinguliHumansMagnetic Resonance SpectroscopyMaleMemoryExcitatory Amino Acid Antagonistsgamma-Aminobutyric AcidGlutamic AcidRiluzole1H-MRS22q11.2DScognitionGABAGlutmateriluzolevoltage-gated sodium channel blocker

Identifiers

PMID32448020
PMCPMC7376622
OpenAlexW3028139256

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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.