Aberrant Salience, Information Processing, and Dopaminergic Signaling in People at Clinical High Risk for Psychosis

The aberrant salience hypothesis proposes that striatal dopamine dysregulation causes misattribution of salience to irrelevant stimuli leading to psychosis. Recently, new lines of preclinical evidence on information coding by subcortical dopamine coupled with computational models of the brain’s abil...

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Published inBiological psychiatry (1969) Vol. 88; no. 4; pp. 304 - 314
Main Authors Howes, Oliver D., Hird, Emily J., Adams, Rick A., Corlett, Philip R., McGuire, Philip
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 15.08.2020
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Online AccessGet full text
ISSN0006-3223
1873-2402
1873-2402
DOI10.1016/j.biopsych.2020.03.012

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Abstract The aberrant salience hypothesis proposes that striatal dopamine dysregulation causes misattribution of salience to irrelevant stimuli leading to psychosis. Recently, new lines of preclinical evidence on information coding by subcortical dopamine coupled with computational models of the brain’s ability to predict and make inferences about the world (predictive processing) provide a new perspective on this hypothesis. We review these and summarize the evidence for dopamine dysfunction, reward processing, and salience abnormalities in people at clinical high risk of psychosis (CHR) relative to findings in patients with psychosis. This review identifies consistent evidence for dysregulated subcortical dopamine function in people at CHR, but also indicates a number of areas where neurobiological processes are different in CHR subjects relative to patients with psychosis, particularly in reward processing. We then consider how predictive processing models may explain psychotic symptoms in terms of alterations in prediction error and precision signaling using Bayesian approaches. We also review the potential role of environmental risk factors, particularly early adverse life experiences, in influencing the prior expectations that individuals have about their world in terms of computational models of the progression from being at CHR to frank psychosis. We identify a number of key outstanding questions, including the relative roles of prediction error or precision signaling in the development of symptoms and the mechanism underlying dopamine dysfunction. Finally, we discuss how the integration of computational psychiatry with biological investigation may inform the treatment for people at CHR of psychosis.
AbstractList The aberrant salience hypothesis proposes that striatal dopamine dysregulation causes misattribution of salience to irrelevant stimuli leading to psychosis. Recently, new lines of preclinical evidence on information coding by subcortical dopamine coupled with computational models of the brain’s ability to predict and make inferences about the world (predictive processing) provide a new perspective on this hypothesis. We review these and summarize the evidence for dopamine dysfunction, reward processing, and salience abnormalities in people at clinical high risk of psychosis (CHR) relative to findings in patients with psychosis. This review identifies consistent evidence for dysregulated subcortical dopamine function in people at CHR, but also indicates a number of areas where neurobiological processes are different in CHR subjects relative to patients with psychosis, particularly in reward processing. We then consider how predictive processing models may explain psychotic symptoms in terms of alterations in prediction error and precision signaling using Bayesian approaches. We also review the potential role of environmental risk factors, particularly early adverse life experiences, in influencing the prior expectations that individuals have about their world in terms of computational models of the progression from being at CHR to frank psychosis. We identify a number of key outstanding questions, including the relative roles of prediction error or precision signaling in the development of symptoms and the mechanism underlying dopamine dysfunction. Finally, we discuss how the integration of computational psychiatry with biological investigation may inform the treatment for people at CHR of psychosis.
The aberrant salience hypothesis proposes that striatal dopamine dysregulation causes misattribution of salience to irrelevant stimuli leading to psychosis. Recently, new lines of preclinical evidence on information coding by subcortical dopamine coupled with computational models of the brain's ability to predict and make inferences about the world (predictive processing) provide a new perspective on this hypothesis. We review these and summarize the evidence for dopamine dysfunction, reward processing, and salience abnormalities in people at clinical high risk of psychosis (CHR) relative to findings in patients with psychosis. This review identifies consistent evidence for dysregulated subcortical dopamine function in people at CHR, but also indicates a number of areas where neurobiological processes are different in CHR subjects relative to patients with psychosis, particularly in reward processing. We then consider how predictive processing models may explain psychotic symptoms in terms of alterations in prediction error and precision signaling using Bayesian approaches. We also review the potential role of environmental risk factors, particularly early adverse life experiences, in influencing the prior expectations that individuals have about their world in terms of computational models of the progression from being at CHR to frank psychosis. We identify a number of key outstanding questions, including the relative roles of prediction error or precision signaling in the development of symptoms and the mechanism underlying dopamine dysfunction. Finally, we discuss how the integration of computational psychiatry with biological investigation may inform the treatment for people at CHR of psychosis.The aberrant salience hypothesis proposes that striatal dopamine dysregulation causes misattribution of salience to irrelevant stimuli leading to psychosis. Recently, new lines of preclinical evidence on information coding by subcortical dopamine coupled with computational models of the brain's ability to predict and make inferences about the world (predictive processing) provide a new perspective on this hypothesis. We review these and summarize the evidence for dopamine dysfunction, reward processing, and salience abnormalities in people at clinical high risk of psychosis (CHR) relative to findings in patients with psychosis. This review identifies consistent evidence for dysregulated subcortical dopamine function in people at CHR, but also indicates a number of areas where neurobiological processes are different in CHR subjects relative to patients with psychosis, particularly in reward processing. We then consider how predictive processing models may explain psychotic symptoms in terms of alterations in prediction error and precision signaling using Bayesian approaches. We also review the potential role of environmental risk factors, particularly early adverse life experiences, in influencing the prior expectations that individuals have about their world in terms of computational models of the progression from being at CHR to frank psychosis. We identify a number of key outstanding questions, including the relative roles of prediction error or precision signaling in the development of symptoms and the mechanism underlying dopamine dysfunction. Finally, we discuss how the integration of computational psychiatry with biological investigation may inform the treatment for people at CHR of psychosis.
AbstractThe aberrant salience hypothesis proposes that striatal dopamine dysregulation causes misattribution of salience to irrelevant stimuli leading to psychosis. Recently, new lines of preclinical evidence on information coding by subcortical dopamine coupled with computational models of the brain’s ability to predict and make inferences about the world (predictive processing) provide a new perspective on this hypothesis. We review these and summarize the evidence for dopamine dysfunction, reward processing, and salience abnormalities in people at clinical high risk of psychosis (CHR) relative to findings in patients with psychosis. This review identifies consistent evidence for dysregulated subcortical dopamine function in people at CHR, but also indicates a number of areas where neurobiological processes are different in CHR subjects relative to patients with psychosis, particularly in reward processing. We then consider how predictive processing models may explain psychotic symptoms in terms of alterations in prediction error and precision signaling using Bayesian approaches. We also review the potential role of environmental risk factors, particularly early adverse life experiences, in influencing the prior expectations that individuals have about their world in terms of computational models of the progression from being at CHR to frank psychosis. We identify a number of key outstanding questions, including the relative roles of prediction error or precision signaling in the development of symptoms and the mechanism underlying dopamine dysfunction. Finally, we discuss how the integration of computational psychiatry with biological investigation may inform the treatment for people at CHR of psychosis.
Author McGuire, Philip
Howes, Oliver D.
Adams, Rick A.
Hird, Emily J.
Corlett, Philip R.
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Keywords Psychosis
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PublicationTitle Biological psychiatry (1969)
PublicationTitleAlternate Biol Psychiatry
PublicationYear 2020
Publisher Elsevier Inc
Publisher_xml – name: Elsevier Inc
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Snippet The aberrant salience hypothesis proposes that striatal dopamine dysregulation causes misattribution of salience to irrelevant stimuli leading to psychosis....
AbstractThe aberrant salience hypothesis proposes that striatal dopamine dysregulation causes misattribution of salience to irrelevant stimuli leading to...
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SubjectTerms Bayes Theorem
Cognition
Computational psychiatry
Dopamine
Humans
Imaging
Prodrome
Psychiatric/Mental Health
Psychosis
Psychotic Disorders
Reward
Risk
Schizophrenia
Title Aberrant Salience, Information Processing, and Dopaminergic Signaling in People at Clinical High Risk for Psychosis
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https://dx.doi.org/10.1016/j.biopsych.2020.03.012
https://www.ncbi.nlm.nih.gov/pubmed/32430200
https://www.proquest.com/docview/2405305686
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