Evidence map›Paper›PMID 26324100›Full record

ArticleMolecular psychiatry2016

High loading of polygenic risk in cases with chronic schizophrenia.

S M Meier, E Agerbo, R Maier, C B Pedersen, M Lang, J Grove, M V Hollegaard, D Demontis, B B Trabjerg, C Hjorthøj and 15 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 4 pooled it
6.9field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 4 syntheses or guidelines pooled it, 76 citations in OpenAlex.

  1. Pooled it
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  12. Assessing the validity of a self-reported clinical diagnosis of schizophrenia.medRxiv : the preprint server for health sciences · 2023
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  20. Pharmacogenetics of Antipsychotic Treatment in Schizophrenia.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
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

25 authors at 9 institutions in 4 countries.

S M MeierNational Centre for Register-Based Research, Aarhus University, Aarhus C, Denmark.
E AgerboNational Centre for Register-Based Research, Aarhus University, Aarhus C, Denmark.ORCID 0000-0002-2849-524X
R MaierQueensland Brain Institute, University of Queensland, Brisbane, Queensland, Australia.
C B PedersenNational Centre for Register-Based Research, Aarhus University, Aarhus C, Denmark.
M LangDepartment of Genetic Epidemiology in Psychiatry, Central Institute of Mental Health, Mannheim, Germany.
J GroveLundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, Denmark.
M V HollegaardDanish Centre for Neonatal Screening, Department of Congenital Disorders, Statens Serum Institut, Copenhagen, Denmark.
D DemontisLundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, Denmark.
B B TrabjergNational Centre for Register-Based Research, Aarhus University, Aarhus C, Denmark.
C HjorthøjLundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, Denmark.
S RipkeAnalytical and Translational Genetics Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.ORCID 0000-0003-3622-835X
F DegenhardtInstitute of Human Genetics, University of Bonn, Bonn, Germany.
M M NöthenInstitute of Human Genetics, University of Bonn, Bonn, Germany.
D RujescuDepartment of Psychiatry, Psychotherapy and Psychosomatics, Martin-Luther-University Halle-Wittenberg, Halle, Germany.
W MaierDepartment of Psychiatry, University of Bonn, Bonn, Germany.
MooDS SCZ Consortium
T WergeLundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, Denmark.
O MorsLundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, Denmark.
D M HougaardDanish Centre for Neonatal Screening, Department of Congenital Disorders, Statens Serum Institut, Copenhagen, Denmark.
A D BørglumLundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, Denmark.
N R WrayQueensland Brain Institute, University of Queensland, Brisbane, Queensland, Australia.
M RietschelDepartment of Genetic Epidemiology in Psychiatry, Central Institute of Mental Health, Mannheim, Germany.
M NordentoftLundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, Denmark.
P B MortensenNational Centre for Register-Based Research, Aarhus University, Aarhus C, Denmark.
M MattheisenLundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, Denmark.
Aarhus University · DKUniversity of Bonn · DEUniversity of Copenhagen · DKCentral Institute of Mental Health · DEStatens Serum Institut · DKThe University of Queensland · AUAarhus University Hospital · DKBroad Institute · USMartin Luther University Halle-Wittenberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genomic risk profile scores (GRPSs) have been shown to predict case-control status of schizophrenia (SCZ), albeit with varying sensitivity and specificity. The extent to which this variability in prediction accuracy is related to differences in sampling strategies is unknown. Danish population-based registers and Neonatal Biobanks were used to identify two independent incident data sets (denoted target and replication) comprising together 1861 cases with SCZ and 1706 controls. A third data set was a German prevalent sample with diagnoses assigned to 1773 SCZ cases and 2161 controls based on clinical interviews. GRPSs were calculated based on the genome-wide association results from the largest SCZ meta-analysis yet conducted. As measures of genetic risk prediction, Nagelkerke pseudo-R(2) and variance explained on the liability scale were calculated. GRPS for SCZ showed positive correlations with the number of psychiatric admissions across all P-value thresholds in both the incident and prevalent samples. In permutation-based test, Nagelkerke pseudo-R(2) values derived from samples enriched for frequently admitted cases were found to be significantly higher than for the full data sets (Ptarget=0.017, Preplication=0.04). Oversampling of frequently admitted cases further resulted in a higher proportion of variance explained on the liability scale (improvementtarget= 50%; improvementreplication= 162%). GRPSs are significantly correlated with chronicity of SCZ. Oversampling of cases with a high number of admissions significantly increased the amount of variance in liability explained by GRPS. This suggests that at least part of the effect of common single-nucleotide polymorphisms is on the deteriorative course of illness.

Indexed as

AdultCase-Control StudiesDenmarkFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyGermanyHumansMaleMultifactorial InheritancePolymorphism, Single NucleotideRisk FactorsSchizophreniaSensitivity and Specificity

Identifiers

PMID26324100
OpenAlexW1221735883

What OpenQuestion holds

Textmetadata
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.