Evidence map›Paper›PMID 25810055›Full record

ReviewSchizophrenia bulletin2015

The role of schizotypy in the study of the etiology of schizophrenia spectrum disorders.

Neus Barrantes-Vidal, Phillip Grant, Thomas R Kwapil

Open access · bronzeAbstract readReview
In one paragraph

Review in Schizophrenia bulletin, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed, 4 pooled it
21.0field-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.

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

144 citing papers in PubMed, 4 syntheses or guidelines pooled it, 329 citations in OpenAlex.

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84 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

3 authors at 3 institutions in 3 countries.

Neus Barrantes-VidalDepartament de Psicologia Clínica i de la Salut, Universitat Autònoma de Barcelona, Spain; University of North Carolina at Greensboro, Greensboro, NC; Centre for Biomedical Research Network on Mental Health (CIBERSAM), Instituto de Salud Carlos III, Madrid, Spain; Sant Pere Claver - Fundació Sanitària, Barcelona, Spain; neus.barrantes@uab.cat.
Phillip GrantJustus-Liebig-University Giessen, Giessen, Germany.
Thomas R KwapilUniversity of North Carolina at Greensboro, Greensboro, NC;
Centro de Investigación Biomédica en Red de Salud Mental · ESUniversity of Giessen · DEUniversity of North Carolina at Greensboro · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schizotypy provides a useful construct for understanding the development of schizophrenia spectrum disorders. As research on the epidemiology of psychotic symptoms and clinical risk for psychosis has expanded, conceptual challenges have emerged to comprehend the nature and borders of the space comprised between personality variation and psychosis. Schizotypy is considered in light of these more recent constructs. It is suggested that rather than being superseded by them due to their higher specificity and predictive power for transition to psychosis, schizotypy integrates them as it constitutes a dynamic continuum ranging from personality to psychosis. The advantages of schizotypy for studying schizophrenia etiology are discussed (eg, it facilitates a developmental approach and the identification of causal, resilience, and compensating factors and offers a multidimensional structure that captures etiological heterogeneity). An overview of putative genetic, biological, and psychosocial risk factors is presented, focusing on communalities and differences between schizotypy and schizophrenia spectrum disorders. The found notable overlap supports etiological continuity, and, simultaneously, differential findings appear that are critical to understanding resilience to schizophrenia. For example, discrepant findings in genetic studies might be interpreted as suggestive of sets of independent genetic factors playing a differential role in schizotypy and schizophrenia: some would influence variation specifically on schizotypy dimensions (ie, high vs low schizotypy, thereby increasing proneness to psychosis), some would confer unspecific liability to disease by impacting neural properties and susceptibility to environmental factors (ie, high vs low resilience to disorder) and some might contribute to disease-specific characteristics. Finally, schizotypy's promise for studying gene-environment interactions is considered.

Indexed as

Gene-Environment InteractionHumansPsychotic DisordersSchizophreniaSchizotypal Personality Disorderenvironmentgeneticspsychosispsychosis pronenesspsychotic-like experiencesrisk factors

Identifiers

PMID25810055
PMCPMC4373635
OpenAlexW2098157189

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.