Evidence map›Paper›PMID 29382821›Full record

ReviewTranslational psychiatry2018

Dopamine, psychosis and schizophrenia: the widening gap between basic and clinical neuroscience.

J P Kesby, D W Eyles, J J McGrath, J G Scott

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Translational psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06856161 (A Novel Blood Test as a Differential Diagnosis and Drug Efficacy Biomarker in Mental Health), which is not on this map. Cited by 166 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
166citing papers in PubMed, 5 pooled it
22.8field-weighted citation impact, top 1% 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.

NCT06856161 recruitingnot on this mapstarted 2025, after this paper: background citation

A Novel Blood Test as a Differential Diagnosis and Drug Efficacy Biomarker in Mental Health

TypeobservationalSponsorFraser HealthRan2025 to 2027Enrolled500ConditionsDepression - Major Depressive Disorder, Schizophenia Disorder, Psychosis, Mania (Neurotic)
3 · Its place in the literature

Who cites it

166 citing papers in PubMed, 5 syntheses or guidelines pooled it, 345 citations in OpenAlex.

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  8. The hippocampus as a generative model.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
    Review
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  20. Stimulation of CaScience signaling · 2025
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106 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 2 countries.

J P KesbyQueensland Brain Institute, The University of Queensland, St. Lucia, QLD, Australia. j.kesby@uq.edu.au.ORCID http://orcid.org/0000-0002-5814-8062
D W EylesQueensland Brain Institute, The University of Queensland, St. Lucia, QLD, Australia.
J J McGrathQueensland Brain Institute, The University of Queensland, St. Lucia, QLD, Australia.ORCID http://orcid.org/0000-0002-4792-6068
J G ScottCentre for Clinical Research, Faculty of Medicine, The University of Queensland, Herston, QLD, Australia.
The University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The stagnation in drug development for schizophrenia highlights the need for better translation between basic and clinical research. Understanding the neurobiology of schizophrenia presents substantial challenges but a key feature continues to be the involvement of subcortical dopaminergic dysfunction in those with psychotic symptoms. Our contemporary knowledge regarding dopamine dysfunction has clarified where and when dopaminergic alterations may present in schizophrenia. For example, clinical studies have shown patients with schizophrenia show increased presynaptic dopamine function in the associative striatum, rather than the limbic striatum as previously presumed. Furthermore, subjects deemed at high risk of developing schizophrenia show similar presynaptic dopamine abnormalities in the associative striatum. Thus, our view of subcortical dopamine function in schizophrenia continues to evolve as we accommodate this newly acquired information. However, basic research in animal models has been slow to incorporate these clinical findings. For example, psychostimulant-induced locomotion, the commonly utilised phenotype for positive symptoms in rodents, is heavily associated with dopaminergic activation in the limbic striatum. This anatomical misalignment has brought into question how we assess positive symptoms in animal models and represents an opportunity for improved translation between basic and clinical research. The current review focuses on the role of subcortical dopamine dysfunction in psychosis and schizophrenia. We present and discuss alternative phenotypes that may provide a more translational approach to assess the neurobiology of positive symptoms in schizophrenia. Incorporation of recent clinical findings is essential if we are to develop meaningful translational animal models.

Indexed as

AnimalsCorpus StriatumDisease Models, AnimalDopamineHumansNeurobiologyPsychotic DisordersSchizophreniaDopamine

Identifiers

PMID29382821
PMCPMC5802623
OpenAlexW2795334944

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.