Evidence map›Paper›PMID 30301944›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2019

Heritability of cerebral glutamate levels and their association with schizophrenia spectrum disorders: a

Christian Stefan Legind, Brian Villumsen Broberg, René Christiaan William Mandl, Rachel Brouwer, Simon Jesper Anhøj, Rikke Hilker, Maria Høj Jensen, Philip McGuire, Hilleke Hulshoff Pol, Birgitte Fagerlund and 2 more

Open access · bronzeAbstract readTwin Study
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 5 pooled it
2.3field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 5 syntheses or guidelines pooled it, 30 citations in OpenAlex.

  1. Pooled it
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  6. Article
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  9. Thalamocortical dysrhythmia in patients with schizophrenia spectrum disorder and individuals at clinical high risk for psychosis.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022
    Article
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  13. Evaluating endophenotypes for bipolar disorder.International journal of bipolar disorders · 2021
    Review
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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 3 institutions in 3 countries.

Christian Stefan LegindCenter for Clinical Intervention and Neuropsychiatric Schizophrenia Research, CINS, & Center for Neuropsychiatric Schizophrenia Research, CNSR, Mental Health Center Glostrup, University of Copenhagen, Copenhagen, Denmark. christian_l@cnsr.dk.ORCID http://orcid.org/0000-0001-7783-3703
Brian Villumsen BrobergCenter for Clinical Intervention and Neuropsychiatric Schizophrenia Research, CINS, & Center for Neuropsychiatric Schizophrenia Research, CNSR, Mental Health Center Glostrup, University of Copenhagen, Copenhagen, Denmark.
René Christiaan William MandlCenter for Clinical Intervention and Neuropsychiatric Schizophrenia Research, CINS, & Center for Neuropsychiatric Schizophrenia Research, CNSR, Mental Health Center Glostrup, University of Copenhagen, Copenhagen, Denmark.
Rachel BrouwerDepartment of Psychiatry, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
Simon Jesper AnhøjCenter for Clinical Intervention and Neuropsychiatric Schizophrenia Research, CINS, & Center for Neuropsychiatric Schizophrenia Research, CNSR, Mental Health Center Glostrup, University of Copenhagen, Copenhagen, Denmark.
Rikke HilkerCenter for Clinical Intervention and Neuropsychiatric Schizophrenia Research, CINS, & Center for Neuropsychiatric Schizophrenia Research, CNSR, Mental Health Center Glostrup, University of Copenhagen, Copenhagen, Denmark.
Maria Høj JensenCenter for Clinical Intervention and Neuropsychiatric Schizophrenia Research, CINS, & Center for Neuropsychiatric Schizophrenia Research, CNSR, Mental Health Center Glostrup, University of Copenhagen, Copenhagen, Denmark.
Philip McGuireDepartment of Psychosis Studies, Institute of Psychiatry, Psychology & Neuroscience (IoPPN), King's College London, De Crespigny Park, London, UK.
Hilleke Hulshoff PolDepartment of Psychiatry, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
Birgitte FagerlundCenter for Clinical Intervention and Neuropsychiatric Schizophrenia Research, CINS, & Center for Neuropsychiatric Schizophrenia Research, CNSR, Mental Health Center Glostrup, University of Copenhagen, Copenhagen, Denmark.
Egill RostrupCenter for Clinical Intervention and Neuropsychiatric Schizophrenia Research, CINS, & Center for Neuropsychiatric Schizophrenia Research, CNSR, Mental Health Center Glostrup, University of Copenhagen, Copenhagen, Denmark.
Birte Yding GlenthøjCenter for Clinical Intervention and Neuropsychiatric Schizophrenia Research, CINS, & Center for Neuropsychiatric Schizophrenia Research, CNSR, Mental Health Center Glostrup, University of Copenhagen, Copenhagen, Denmark.
University of Copenhagen · DKUtrecht University · NLKing's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Research findings implicate cerebral glutamate in the pathophysiology of schizophrenia, including genetic studies reporting associations with glutamatergic neurotransmission. The extent to which aberrant glutamate levels can be explained by genetic factors is unknown, and if glutamate can serve as a marker of genetic susceptibility for schizophrenia remains to be established. We investigated the heritability of cerebral glutamate levels and whether a potential association with schizophrenia spectrum disorders could be explained by genetic factors. Twenty-three monozygotic (MZ) and 20 dizygotic (DZ) proband pairs con- or discordant for schizophrenia spectrum disorders, along with healthy control pairs (MZ = 28, DZ = 18) were recruited via the National Danish Twin Register and the Psychiatric Central Register (17 additional twins were scanned without their siblings). Glutamate levels in the left thalamus and the anterior cingulate cortex (ACC) were measured using 1[H]-magnetic resonance spectroscopy at 3 Tesla and analyzed by structural equation modeling. Glutamate levels in the left thalamus were heritable and positively correlated with liability for schizophrenia spectrum disorders (phenotypic correlation, 0.16, [0.02-0.29]; p = 0.010). The correlation was explained by common genes influencing both the levels of glutamate and liability for schizophrenia spectrum disorders. In the ACC, glutamate and glx levels were heritable, but not correlated to disease liability. Increases in thalamic glutamate levels found in schizophrenia spectrum disorders are explained by genetic influences related to the disease, and as such the measure could be a potential marker of genetic susceptibility, useful in early detection and stratification of patients with psychosis.

Indexed as

RegistriesAdultDenmarkFemaleGenetic Predisposition to DiseaseGlutamic AcidGyrus CinguliHumansMaleMiddle AgedProton Magnetic Resonance SpectroscopySchizophreniaThalamusGlutamic Acid

Identifiers

PMID30301944
PMCPMC6333786
OpenAlexW2896600824

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.