Evidence map›Paper›PMID 40037822›Full record

ArticleSchizophrenia bulletin2025

Schizotypy, Psychosis Proneness, and the Polygenic Risk for Schizophrenia and Resilience.

Tina Meller, Clara Lundberg, Carlo Maj, Per Hoffmann, Andreas J Forstner, Markus M Nöthen, Igor Nenadić

Abstract read
In one paragraph

Article in Schizophrenia bulletin, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
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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

7 authors.

Tina MellerCognitive Neuropsychiatry Laboratory, Department of Psychiatry and Psychotherapy, Philipps Universität Marburg, Marburg 35039, Germany.
Clara LundbergCognitive Neuropsychiatry Laboratory, Department of Psychiatry and Psychotherapy, Philipps Universität Marburg, Marburg 35039, Germany.
Carlo MajCenter for Human Genetics, Philipps Universität Marburg, Marburg, Germany.
Per HoffmannInstitute of Human Genetics, University of Bonn, School of Medicine & University Hospital Bonn, Bonn, Germany.
Andreas J ForstnerCenter for Human Genetics, Philipps Universität Marburg, Marburg, Germany.
Markus M NöthenInstitute of Human Genetics, University of Bonn, School of Medicine & University Hospital Bonn, Bonn, Germany.
Igor NenadićCognitive Neuropsychiatry Laboratory, Department of Psychiatry and Psychotherapy, Philipps Universität Marburg, Marburg 35039, Germany.ORCID 0000-0002-0749-7473

Funding

Deutsche Forschungsgemeinschaft NE2254/1-2Forschungscampus Mittelhessen (FCMH) FlexiFunds 2017_2_1_5University Hospital Giessen and Marburg 11/2017 MR
6 · The paper itself

Abstract

background and hypothesisSchizotypy is a well-established phenotype for psychosis proneness and risk. Yet, its genetic underpinnings and relations to genetic bases of the schizophrenia spectrum are not well understood owing to conflicting findings. In a deep phenotyping approach, we hypothesized that genetic markers of risk for and to schizophrenia are differentially associated with (trait-level) dimensions of schizotypy and (state-level) prodromal symptoms. STUDY

designIn 367 (130 male, 237 female) psychiatrically healthy young adults, we assessed multiple schizotypy instruments (OLIFE, SPQ-B, Multidimensional Schizotypy Scales), aggregated into composite scores, and a measure of prodromal symptoms (PQ-16). Those were tested for direct and interactive associations with the polygenic risk score (PRS) for schizophrenia and a novel PRS for resilience to schizophrenia. STUDY

resultsBoth prodromal symptom number (rho = 0.16, pcorr = .018) and distress (rho = 0.14, pcorr = .027) were positively related to the schizophrenia PRS. Positive schizotypy showed a similar association but did not remain significant after correction (rho = 0.11, pcorr = .082). Schizophrenia PRS and disorganized schizotypy had a negative interactive effect on prodromal symptom distress (b = -0.10, pcorr = .048). The resilience score did not show any significant associations with any of the measures.

conclusionsThese results further support the idea of a (partially) shared genetic basis of schizophrenia and nonclinical, predominantly positive expressions of the psychosis spectrum but also indicate relevant distinctions between the 2, possibly related to other modulating factors or general (transdiagnostic) psychopathological risk. In line with previous findings, effects seem to be more robust for state- than trait-level markers, but these may also be influencing each other.

Indexed as

Genetic Predisposition to DiseaseMultifactorial InheritanceProdromal SymptomsPsychotic DisordersResilience, PsychologicalSchizophreniaSchizotypal Personality DisorderAdolescentAdultFemaleHumansMaleYoung Adultdeep phenotypingdistressgeneticspolygenic risk score (PRS)prodromal symptomsresilienceschizophreniaschizotypy

Identifiers

PMID40037822
PMCPMC11879570

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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.