Evidence map›Paper›PMID 39145348›Full record

ArticleSchizophrenia bulletin open2023

Hippocampal Glutamate, Resting Perfusion and the Effects of Cannabidiol in Psychosis Risk.

Cathy Davies, Matthijs G Bossong, Daniel Martins, Robin Wilson, Elizabeth Appiah-Kusi, Grace Blest-Hopley, Paul Allen, Fernando Zelaya, David J Lythgoe, Michael Brammer and 3 more

Abstract read
In one paragraph

Article in Schizophrenia bulletin open, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. Review
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

13 authors.

Cathy DaviesDepartment of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.ORCID https://orcid.org/0000-0003-3011-8643
Matthijs G BossongDepartment of Psychiatry, University Medical Center Utrecht Brain Center, Utrecht University, Utrecht, The Netherlands.
Daniel MartinsDepartment of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Robin WilsonDepartment of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Elizabeth Appiah-KusiDepartment of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.ORCID https://orcid.org/0000-0003-4249-5091
Grace Blest-HopleyDepartment of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Paul AllenDepartment of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Fernando ZelayaDepartment of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
David J LythgoeDepartment of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Michael BrammerDepartment of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Jesus PerezCAMEO Early Intervention Service, Cambridgeshire and Peterborough NHS Foundation Trust, Cambridge, UK.
Philip McGuireDepartment of Psychiatry, University of Oxford, Oxford, UK.
Sagnik BhattacharyyaDepartment of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.

Funding

Medical Research Council MR/J012149/1
6 · The paper itself

Abstract

Background: Preclinical and human data suggest that psychosis onset involves hippocampal glutamatergic dysfunction, driving hyperactivity and hyperperfusion in a hippocampal-midbrain-striatal circuit. Whether glutamatergic dysfunction is related to cerebral perfusion in patients at clinical high risk (CHR) for psychosis, and whether cannabidiol (CBD) has ameliorative effects on glutamate or its relationship with perfusion remains unknown. Methods: Using a double-blind, parallel-group design, 33 CHR patients were randomized to a single 600 mg dose of CBD or placebo; 19 healthy controls did not receive any drug. Proton magnetic resonance spectroscopy was used to measure glutamate concentrations in left hippocampus. We examined differences relating to CHR status (controls vs placebo), effects of CBD (placebo vs CBD), and linear between-group effects, such that placebo>CBD>controls or controls>CBD>placebo. We also examined group × glutamate × cerebral perfusion (measured using Arterial Spin Labeling) interactions. Results: Compared to controls, CHR-placebo patients had significantly lower hippocampal glutamate ( Conclusions: Our findings suggest that hippocampal glutamate is lower in CHR patients and may be partially normalized by a single dose of CBD. Furthermore, we provide the first in vivo evidence of an abnormal relationship between hippocampal glutamate and perfusion in the striatum and insula in CHR.

Indexed as

at-risk mental statecerebral blood flowclinical high risk for psychosismagnetic resonance spectroscopy

Identifiers

PMID39145348
PMCPMC11207663

What Socratic 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 Socratic graph.