Evidence map›Paper›PMID 30171181›Full record

ArticleTranslational psychiatry2018

Polygenic risk score analyses of symptoms and treatment response in an antipsychotic-naive first episode of psychosis cohort.

Marcos Leite Santoro, Vanessa Ota, Simone de Jong, Cristiano Noto, Leticia M Spindola, Fernanda Talarico, Eduardo Gouvea, Sang Hyuck Lee, Patricia Moretti, Charles Curtis and 8 more

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

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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

18 authors at 3 institutions in 2 countries.

Marcos Leite SantoroGenetics Division, Federal University of São Paulo (UNIFESP), São Paulo, SP, Brazil.
Vanessa OtaGenetics Division, Federal University of São Paulo (UNIFESP), São Paulo, SP, Brazil.
Simone de JongSocial, Genetics & Developmental Psychiatry Centre (SGDP), Institute of Psychiatry, Psychology and Neuroscience at King's College London, London, UK.
Cristiano NotoDepartment of Psychiatry, Federal University of São Paulo (UNIFESP), São Paulo, SP, Brazil.
Leticia M SpindolaInterdisciplinary Laboratory of Clinical Neurosciences, Federal University of São Paulo (UNIFESP), São Paulo, SP, Brazil.
Fernanda TalaricoInterdisciplinary Laboratory of Clinical Neurosciences, Federal University of São Paulo (UNIFESP), São Paulo, SP, Brazil.
Eduardo GouveaDepartment of Psychiatry, Federal University of São Paulo (UNIFESP), São Paulo, SP, Brazil.
Sang Hyuck LeeSocial, Genetics & Developmental Psychiatry Centre (SGDP), Institute of Psychiatry, Psychology and Neuroscience at King's College London, London, UK.
Patricia MorettiInterdisciplinary Laboratory of Clinical Neurosciences, Federal University of São Paulo (UNIFESP), São Paulo, SP, Brazil.
Charles CurtisSocial, Genetics & Developmental Psychiatry Centre (SGDP), Institute of Psychiatry, Psychology and Neuroscience at King's College London, London, UK.
Hamel PatelSocial, Genetics & Developmental Psychiatry Centre (SGDP), Institute of Psychiatry, Psychology and Neuroscience at King's College London, London, UK.
Stephen NewhouseSocial, Genetics & Developmental Psychiatry Centre (SGDP), Institute of Psychiatry, Psychology and Neuroscience at King's College London, London, UK.ORCID http://orcid.org/0000-0002-1843-9842
Carolina Muniz CarvalhoInterdisciplinary Laboratory of Clinical Neurosciences, Federal University of São Paulo (UNIFESP), São Paulo, SP, Brazil.
Ary GadelhaInterdisciplinary Laboratory of Clinical Neurosciences, Federal University of São Paulo (UNIFESP), São Paulo, SP, Brazil.
Quirino CordeiroDepartment of Psychiatry, Federal University of São Paulo (UNIFESP), São Paulo, SP, Brazil.
Rodrigo Affonseca BressanInterdisciplinary Laboratory of Clinical Neurosciences, Federal University of São Paulo (UNIFESP), São Paulo, SP, Brazil.
Sintia Iole BelangeroGenetics Division, Federal University of São Paulo (UNIFESP), São Paulo, SP, Brazil.
Gerome BreenSocial, Genetics & Developmental Psychiatry Centre (SGDP), Institute of Psychiatry, Psychology and Neuroscience at King's College London, London, UK. gerome.breen@gmail.com.
Universidade Federal de São Paulo · BRKing's College London · GBIrmandade da Santa Casa de Misericórdia de São Paulo · BR

Funding

Department of HealthMedical Research Council MR/M026337/1
6 · The paper itself

Abstract

In this study, we aimed to test if the schizophrenia (SCZ) polygenic risk score (PRS) was associated with clinical symptoms in (a) the first episode of psychosis pre-treatment (FEP), (b) at nine weeks after initiation of risperidone treatment (FEP-9W) and (c) with the response to risperidone. We performed a detailed clinical assessment of 60 FEP patients who were antipsychotic-naive and, again, after nine weeks of standardized treatment with risperidone. After blood collection and DNA isolation, the samples were genotyped using the Illumina PsychArrayChip and then imputed. To calculate PRS, we used the latest available GWAS summary statistics from the Psychiatric Genomics Consortium wave-2 SCZ group as a training set. We used Poisson regression to test association between PRS and clinical measurements correcting for the four principal components (genotyping). We considered a p-value < 0.0014 (Bonferroni correction) as significant. First, we verified that the schizophrenia PRS was also able to distinguish cases from controls in this south-eastern Brazilian sample, with a similar variance explained to that seen in Northern European populations. In addition, within-cases analyses, we found that PRS is significantly correlated with baseline (pre-treatment) symptoms, as measured by lower clinical global assessment of functioning (-GAF), higher depressive symptoms and higher scores on a derived excitement factor. After standardized treatment for nine weeks, the correlation with GAF and the excitement factor disappeared while depressive symptoms became negatively associated with PRS. We conclude that drug (and other treatments) may confound attempts to understand the aetiological influence on symptomatology of polygenic risk scores. These results highlight the importance of studying schizophrenia, and other disorders, pre-treatment to understand the relationship between polygenic risk and phenotypic features.

Indexed as

Genetic Predisposition to DiseaseAdolescentAdultAntipsychotic AgentsBrazilCase-Control StudiesFemaleHumansLongitudinal StudiesMaleMultifactorial InheritancePolymorphism, Single NucleotidePsychiatric Status Rating ScalesRisk AssessmentRisperidoneSchizophreniaAntipsychotic AgentsRisperidone

Identifiers

PMID30171181
PMCPMC6119191
OpenAlexW2889271113

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.