ArticleNature medicine2018
Convergence of placenta biology and genetic risk for schizophrenia.
Article in Nature medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
142 citing papers in PubMed, 1 synthesis or guideline pooled it, 285 citations in OpenAlex.
- Vitamin D and schizophrenia: 20 years on.Molecular psychiatry · 2021Pooled it
- Relationships between early age at onset of psychotic symptoms and treatment resistant schizophrenia.Early intervention in psychiatry · 2022Trial
- Mapping the psychosis spectrum - imaging neurosubtypes from multiscale functional network connectivity.Molecular psychiatry · 2026Article
- Perinatal insults, genetic susceptibility, and the pathogenesis of neurodevelopmental disorders: from epigenetic remodeling to neural circuit dysfunction-a narrative review.Translational pediatrics · 2026Review
- Developmental and cellular vulnerabilities underlie genetic architecture of schizophrenia.Molecular psychiatry · 2026Article
- Long-read assembly reveals vast transcriptional complexity in the placenta associated with metabolic and endocrine function.Nature communications · 2026Article
- Reelin regulates the migration and differentiation of extravillous trophoblastic cells.Biological research · 2026Article
- Prenatal Adversities and Risk of Persistent Youth Psychopathology and Altered Cortical Thinning.JAMA psychiatry · 2026Article
- Biological underpinnings and genetic predisposition to schizophrenia within microrna-137 regulatory pathways across brain development.Translational psychiatry · 2026Article
- Identifying established human placental markers of schizophrenia in rodents after gestational ∆9-tetrahydrocannabinol exposure†.Biology of reproduction · 2026Article
- Synergistic pathways to psychosis: understanding developmental risk and resilience factors.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Review
- Transdiagnostic prevention in youth mental health, Part I: rationale, shared risk factors.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Review
- Schizophrenia.Nature reviews. Disease primers · 2025Review
- Unraveling the mysteries of schizophrenia: Insights into prefrontal cortex dysfunction and therapeutic implications.World journal of psychiatry · 2025Review
- Molecular Signatures of Schizophrenia and Insights into Potential Biological Convergence.International journal of molecular sciences · 2025Review
- Epiphenomena in psychosis: how perinatal stressful events shape long-term outcomes.Molecular psychiatry · 2025Review
- Association of Adverse Prenatal Exposure Burden with Persistent Psychopathology and Accelerated Cortical Thinning in Youth.medRxiv : the preprint server for health sciences · 2025Article
- Obstetric complications, cortical gyrification, and cognition in first-episode psychosis.Psychological medicine · 2025Article
- Neuroactive steroid exposure impacts neurodevelopment: Comparison of human and rodent placental contribution.Journal of neuroendocrinology · 2025Review
- From Womb to Mind: Prenatal Epigenetic Influences on Mental Health Disorders.International journal of molecular sciences · 2025Review
82 more citing papers are in PubMed but not listed here.
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Authors and funding
23 authors at 9 institutions in 5 countries.
Funding
Abstract
Defining the environmental context in which genes enhance disease susceptibility can provide insight into the pathogenesis of complex disorders. We report that the intra-uterine environment modulates the association of schizophrenia with genomic risk (in this study, genome-wide association study-derived polygenic risk scores (PRSs)). In independent samples from the United States, Italy, and Germany, the liability of schizophrenia explained by PRS is more than five times greater in the presence of early-life complications (ELCs) compared with their absence. Patients with ELC histories have significantly higher PRS than patients without ELC histories, which is confirmed in additional samples from Germany and Japan. The gene set composed of schizophrenia loci that interact with ELCs is highly expressed in placenta, is differentially expressed in placentae from complicated in comparison with normal pregnancies, and is differentially upregulated in placentae from male compared with female offspring. Pathway analyses reveal that genes driving the PRS-ELC interaction are involved in cellular stress response; genes that do not drive such interaction implicate orthogonal biological processes (for example, synaptic function). We conclude that a subset of the most significant genetic variants associated with schizophrenia converge on a developmental trajectory sensitive to events that affect the placental response to stress, which may offer insights into sex biases and primary prevention.
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Registered trials
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.