Evidence map›Paper›PMID 42691140›Full record

ArticleSchizophrenia bulletin2026

A Dual Prediction Error Populations Model of Schizophrenia Spectrum Disorders: Bridging NMDA Hypofunction and Gain Hyperfunction.

Shunsuke Sato, Tadahumi Kato, Taro Toyoizumi

Abstract read
In one paragraph

Article in Schizophrenia bulletin, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Shunsuke SatoSeijin Hospital, Adachi-Ku, Tokyo 121-8515, Japan.ORCID 0009-0008-7795-7878
Tadahumi KatoDepartment of Psychiatry and Behavioral Science, Juntendo University Graduate School of Medicine, Bunkyo-Ku, Tokyo 113-8421, Japan.
Taro ToyoizumiLaboratory for Neural Computation and Adaptation, RIKEN Center for Brain Science, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan.ORCID 0000-0001-5444-8829

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and hypothesisSchizophrenia spectrum disorders (SSDs) span heterogeneous clinical states, from rapidly fluctuating psychosis to rigid, systematized delusions.1 NMDA receptor hypofunction on inhibitory interneurons,2-4 dopaminergic dysregulation,5 and abnormalities of volatility estimation6-10 or precision weighting11-13 have all been implicated, yet a framework linking these mechanisms to spectrum-level heterogeneity remains incomplete. STUDY

designWe developed a biologically plausible predictive-coding model with separable positive and negative prediction error (PE) populations. For clarity, the main text presents a one-dimensional linear Kalman filter. STUDY

resultsNMDA hypofunction selectively weakened negative PE, thereby reducing disconfirmatory updating and biasing inference toward prior-consistent interpretations. Gain hyperfunction amplified precision-weighted updating and produced observation-dominated instability. Their interaction reproduced attenuated mismatch responses, reduced illusion susceptibility, and a bias-volatility plane spanning rigid and unstable delusional dynamics.

conclusionsThe model suggests that SSD heterogeneity can be understood as an interaction between sign-selective bias and abnormal precision weighting. This offers a circuit-to-symptom framework and motivates stratification by the asymmetry and overall gain of PE responses.

Indexed as

DelusionsModels, NeurologicalPsychotic DisordersReceptors, N-Methyl-D-AspartateSchizophreniaHumansReceptors, N-Methyl-D-AspartateBias–volatility spectrumcomputational psychiatryEbbinghaus illusionKalman filtermismatch negativityprecision weighting

Identifiers

PMID42691140
PMCPMC13540744

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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.