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Interaction Testing and Polygenic Risk Scoring to Estimate the Association of Common Genetic Variants With Treatment Resistance in Schizophrenia
AF. Pardiñas, SE. Smart, IR. Willcocks, PA. Holmans, CA. Dennison, AJ. Lynham, SE. Legge, BT. Baune, TB. Bigdeli, MJ. Cairns, A. Corvin, AH. Fanous, J. Frank, B. Kelly, A. McQuillin, I. Melle, PB. Mortensen, BJ. Mowry, CN. Pato, S. Periyasamy, M....
Language English Country United States
Document type Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't
Grant support
052247
Wellcome Trust - United Kingdom
R01 MH104964
NIMH NIH HHS - United States
G0500817
Medical Research Council - United Kingdom
MR/L011794/1
Medical Research Council - United Kingdom
MR/L010305/1
Medical Research Council - United Kingdom
G0801418
Medical Research Council - United Kingdom
R01 MH124873
NIMH NIH HHS - United States
U01 MH109528
NIMH NIH HHS - United States
042025
Wellcome Trust - United Kingdom
R01 MH123451
NIMH NIH HHS - United States
MR/P005748/1
Medical Research Council - United Kingdom
R01 MH077139
NIMH NIH HHS - United States
PDF-2018-11-ST2-020
Department of Health - United Kingdom
Wellcome Trust - United Kingdom
MC_PC_17212
Medical Research Council - United Kingdom
- MeSH
- Genome-Wide Association Study MeSH
- Genetic Predisposition to Disease genetics MeSH
- Humans MeSH
- Multifactorial Inheritance genetics MeSH
- Psychotic Disorders * drug therapy MeSH
- Schizophrenia * diagnosis drug therapy genetics MeSH
- Check Tag
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Research Support, N.I.H., Extramural MeSH
IMPORTANCE: About 20% to 30% of people with schizophrenia have psychotic symptoms that do not respond adequately to first-line antipsychotic treatment. This clinical presentation, chronic and highly disabling, is known as treatment-resistant schizophrenia (TRS). The causes of treatment resistance and their relationships with causes underlying schizophrenia are largely unknown. Adequately powered genetic studies of TRS are scarce because of the difficulty in collecting data from well-characterized TRS cohorts. OBJECTIVE: To examine the genetic architecture of TRS through the reassessment of genetic data from schizophrenia studies and its validation in carefully ascertained clinical samples. DESIGN, SETTING, AND PARTICIPANTS: Two case-control genome-wide association studies (GWASs) of schizophrenia were performed in which the case samples were defined as individuals with TRS (n = 10 501) and individuals with non-TRS (n = 20 325). The differences in effect sizes for allelic associations were then determined between both studies, the reasoning being such differences reflect treatment resistance instead of schizophrenia. Genotype data were retrieved from the CLOZUK and Psychiatric Genomics Consortium (PGC) schizophrenia studies. The output was validated using polygenic risk score (PRS) profiling of 2 independent schizophrenia cohorts with TRS and non-TRS: a prevalence sample with 817 individuals (Cardiff Cognition in Schizophrenia [CardiffCOGS]) and an incidence sample with 563 individuals (Genetics Workstream of the Schizophrenia Treatment Resistance and Therapeutic Advances [STRATA-G]). MAIN OUTCOMES AND MEASURES: GWAS of treatment resistance in schizophrenia. The results of the GWAS were compared with complex polygenic traits through a genetic correlation approach and were used for PRS analysis on the independent validation cohorts using the same TRS definition. RESULTS: The study included a total of 85 490 participants (48 635 [56.9%] male) in its GWAS stage and 1380 participants (859 [62.2%] male) in its PRS validation stage. Treatment resistance in schizophrenia emerged as a polygenic trait with detectable heritability (1% to 4%), and several traits related to intelligence and cognition were found to be genetically correlated with it (genetic correlation, 0.41-0.69). PRS analysis in the CardiffCOGS prevalence sample showed a positive association between TRS and a history of taking clozapine (r2 = 2.03%; P = .001), which was replicated in the STRATA-G incidence sample (r2 = 1.09%; P = .04). CONCLUSIONS AND RELEVANCE: In this GWAS, common genetic variants were differentially associated with TRS, and these associations may have been obscured through the amalgamation of large GWAS samples in previous studies of broadly defined schizophrenia. Findings of this study suggest the validity of meta-analytic approaches for studies on patient outcomes, including treatment resistance.
Baker Heart and Diabetes Institute Melbourne Australia
Centre for Brain and Mental Health Research University of Newcastle Newcastle Australia
College of Pharmacy University of Manitoba Winnipeg Manitoba Canada
Department of Genetics University of North Carolina Chapel Hill
Department of Medical Epidemiology and Biostatistics Karolinska Institutet Stockholm Sweden
Department of Medicine and Psychiatry School of Medicine University of Cantabria Santander Spain
Department of Psychiatry Icahn School of Medicine Mount Sinai Hospital New York New York
Department of Psychiatry Istanbul University Istanbul Turkey
Department of Psychiatry Melbourne Medical School The University of Melbourne Melbourne Australia
Department of Psychiatry University of Münster Münster Germany
Department of Psychiatry Veterans Affairs New York Harbor Healthcare System Brooklyn
Division of Psychiatry Imperial College London London United Kingdom
Faculty of Social Sciences Department of Psychology Beykoz University Istanbul Turkey
Hunter Medical Research Institute Newcastle Australia
Institute for Genomic Health State University of New York Downstate Medical Center Brooklyn
Institute of Medical Sciences University of Aberdeen Aberdeen United Kingdom
Institute of Pharmaceutical Sciences of Western Switzerland University of Geneva Geneva Switzerland
National Centre for Register based Research Aarhus University Aarhus Denmark
Queensland Brain Institute The University of Queensland Brisbane Australia
Queensland Centre for Mental Health Research The University of Queensland Brisbane Australia
School of Biomedical Sciences and Pharmacy University of Newcastle Newcastle Australia
School of Medicine and Public Health The University of Newcastle Newcastle Australia
School of Pharmaceutical Sciences University of Geneva Geneva Switzerland
The Lundbeck Foundation Initiative for Integrative Psychiatric Research Aarhus Denmark
UCL Queen Square Institute of Neurology University College London London United Kingdom
References provided by Crossref.org
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