Evidence map›Paper›PMID 32389614›Full record

ArticleSchizophrenia research2020

Reinforcement learning as an intermediate phenotype in psychosis? Deficits sensitive to illness stage but not associated with polygenic risk of schizophrenia in the general population.

Marcella Montagnese, Franziska Knolle, Joost Haarsma, Juliet D Griffin, Alex Richards, Petra E Vertes, Beatrix Kiddle, Paul C Fletcher, Peter B Jones, Michael J Owen and 7 more

Open access · hybridAbstract read
In one paragraph

Article in Schizophrenia research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
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  11. Neural Circuitry of Salience and Reward Processing in Psychosis.Biological psychiatry global open science · 2023
    Review
  12. Article
  13. The prediction-error hypothesis of schizophrenia: new data point to circuit-specific changes in dopamine activity.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022
    Review
  14. Article
  15. Article
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

17 authors at 5 institutions in 1 country.

Marcella MontagneseDepartment of Psychiatry, University of Cambridge, United Kingdom.
Franziska KnolleDepartment of Psychiatry, University of Cambridge, United Kingdom.
Joost HaarsmaDepartment of Psychiatry, University of Cambridge, United Kingdom.
Juliet D GriffinDepartment of Psychiatry, University of Cambridge, United Kingdom.
Alex RichardsMRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, UK.
Petra E VertesDepartment of Psychiatry, University of Cambridge, United Kingdom.
Beatrix KiddleDepartment of Psychiatry, University of Cambridge, United Kingdom.
Paul C FletcherDepartment of Psychiatry, University of Cambridge, United Kingdom; Wellcome Trust MRC Institute of Metabolic Science, Cambridge, Biomedical Campus, United Kingdom; Cambridgeshire and Peterborough National Health Service Foundation Trust, Cambridge,United Kingdom.
Peter B JonesDepartment of Psychiatry, University of Cambridge, United Kingdom; Cambridgeshire and Peterborough National Health Service Foundation Trust, Cambridge,United Kingdom.
Michael J OwenMRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, UK.
Peter FonagyResearch Department of Clinical, Educational and Health Psychology, University College London, United Kingdom.
Edward T BullmoreDepartment of Psychiatry, University of Cambridge, United Kingdom; Behavioural and Clinical Neuroscience Institute, University of Cambridge, United Kingdom; Cambridgeshire and Peterborough National Health Service Foundation Trust, Cambridge,United Kingdom.
Raymond J DolanMax Planck University College London Centre for Computational Psychiatry and Ageing Research, United Kingdom; Wellcome Centre for Human Neuroimaging, University College London, United Kingdom.
NSPN Consortium
Michael MoutoussisMax Planck University College London Centre for Computational Psychiatry and Ageing Research, United Kingdom; Wellcome Centre for Human Neuroimaging, University College London, United Kingdom.
Ian M GoodyerDepartment of Psychiatry, University of Cambridge, United Kingdom; Cambridgeshire and Peterborough National Health Service Foundation Trust, Cambridge,United Kingdom.
Graham K MurrayDepartment of Psychiatry, University of Cambridge, United Kingdom; Behavioural and Clinical Neuroscience Institute, University of Cambridge, United Kingdom; Cambridgeshire and Peterborough National Health Service Foundation Trust, Cambridge,United Kingdom. Electronic address: gm285@cam.ac.uk.
University of Cambridge · GBNational Health Service · GBCardiff University · GBWellcome Centre for Human Neuroimaging · GBUniversity College London · GB

Funding

Medical Research Council MC_G0802534Wellcome Trust
6 · The paper itself

Abstract

backgroundSchizophrenia is a complex disorder in which the causal relations between risk genes and observed clinical symptoms are not well understood and the explanatory gap is too wide to be clarified without considering an intermediary level. Thus, we aimed to test the hypothesis of a pathway from molecular polygenic influence to clinical presentation occurring via deficits in reinforcement learning.

methodsWe administered a reinforcement learning task (Go/NoGo) that measures reinforcement learning and the effect of Pavlovian bias on decision making. We modelled the behavioural data with a hierarchical Bayesian approach (hBayesDM) to decompose task performance into its underlying learning mechanisms. Study 1 included controls (n = 29, F|M = 0.81), At Risk Mental State for psychosis (ARMS, n = 23, F|M = 0.35) and FEP (First-episode psychosis, n = 26, F|M = 0.18). Study 2 included healthy adolescents (n = 735, F|M = 1.06), 390 of whom had their polygenic risk scores for schizophrenia (PRSs) calculated.

resultsPatients with FEP showed significant impairments in overriding Pavlovian conflict, a lower learning rate and a lower sensitivity to both reward and punishment. Less widespread deficits were observed in ARMS. PRSs did not significantly predict performance on the task in the general population, which only partially correlated with measures of psychopathology.

conclusionsReinforcement learning deficits are observed in first episode psychosis and, to some extent, in those at clinical risk for psychosis, and were not predicted by molecular genetic risk for schizophrenia in healthy individuals. The study does not support the role of reinforcement learning as an intermediate phenotype in psychosis.

Indexed as

Psychotic DisordersSchizophreniaAdolescentBayes TheoremHumansMultifactorial InheritancePhenotypeBayesianComputational psychiatryGo/NoGo taskPRSPsychosisReinforcement learningSchizophrenia

Identifiers

PMID32389614
PMCPMC7594641
OpenAlexW3018331763

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.