ArticleSchizophrenia bulletin2022
Lack of Support for the Genes by Early Environment Interaction Hypothesis in the Pathogenesis of Schizophrenia.
Article in Schizophrenia bulletin, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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.
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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.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Genetic Pathways Point to the Biology Underlying the Association Between Cannabis Use Disorder and Psychosis.Biological psychiatry global open science · 2026Article
- Polygenic and Polyenvironment Interplay in Schizophrenia-Spectrum Disorder and Affective Psychosis; the EUGEI First Episode Study.Schizophrenia bulletin · 2025Article
- Recent findings and future directions for the intersection of genetic and environmental contributions to schizophrenia.Genomic psychiatry : advancing science from genes to society · 2025Article
- A Genome-Wide Association Study of First-Episode Psychosis: A Genetic Exploration in an Italian Cohort.Genes · 2025Article
- Demographic, Premorbid, and Clinical Characteristics of Schizophrenia Spectrum Patients with High and Low Polygenic Liability to the Disorder.Diseases (Basel, Switzerland) · 2025Article
- Stress, Environment and Early Psychosis.Current neuropharmacology · 2024Review
- Exploring the causal effect of placental physiology in susceptibility to mental and addictive disorders: a Mendelian randomization study.Frontiers in psychiatry · 2024Article
- High-throughput screening of glucocorticoid-induced enhancer activity reveals mechanisms of stress-related psychiatric disorders.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The impact of placental genomic risk for schizophrenia and birth asphyxia on brain development.Translational psychiatry · 2023Article
- Prioritization of potential causative genes for schizophrenia in placenta.Nature communications · 2023Article
- Study protocol of the Berlin Research Initiative for Diagnostics, Genetics and Environmental Factors in Schizophrenia (BRIDGE-S).BMC psychiatry · 2023Article
- Infections During Pregnancy and Risks for Adult Psychosis: Findings from the New England Family Study.Current topics in behavioral neurosciences · 2023Article
- The Jury Is Still out on Placental Genes and Obstetric Complications.Schizophrenia bulletin · 2022Article
- Replicating G × E: The Devil and the Details.Schizophrenia bulletin · 2022Article
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- Environmental Risk Factors for Schizophrenia and Bipolar Disorder and Their Relationship to Genetic Risk: Current Knowledge and Future Directions.Frontiers in genetics · 2021Review
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18 authors at 6 institutions in 4 countries.
Funding
Abstract
Ursini et al reported recently that the liability of schizophrenia explained by a polygenic risk score (PRS) derived from the variants most associated with schizophrenia was increased 5-fold in individuals who experienced complications during pregnancy or birth. Follow-up gene expression analysis showed that the genes mapping to the most associated genetic variants are highly expressed in placental tissues. If confirmed, these findings will have major implications in our understanding of the joint effect of genes and environment in the pathogenesis of schizophrenia. We examined the interplay between PRS and obstetric complications (OCs) in 5 independent samples (effective N = 2110). OCs were assessed with the full or modified Lewis-Murray scale, or with birth weight < 2.5 kg as a proxy. In a large cohort we tested whether the pathways from placenta-relevant variants in the original report were associated with case-control status. Unlike in the original study, we did not find significant effect of PRS on the presence of OCs in cases, nor a substantial difference in the association of PRS with case-control status in samples stratified by the presence of OCs. Furthermore, none of the PRS by OCs interactions were significant, nor were any of the biological pathways, examined in the Swedish cohort. Our study could not support the hypothesis of a mediating effect of placenta biology in the pathway from genes to schizophrenia. Methodology differences, in particular the different scales measuring OCs, as well as power constraints for interaction analyses in both studies, may explain this discrepancy.
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