ArticleNature communications2025
Potentially causal associations between placental DNA methylation and schizophrenia and other neuropsychiatric disorders.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Placental DNA methylation captures shared and trait-specific genetic susceptibility across complex health conditions.medRxiv : the preprint server for health sciences · 2026Article
- DNA methylation in the placenta and household socioeconomic status: the SPAH study.Clinical epigenetics · 2026Article
- DNA Methylation-Regulated ZDHHC24 Exacerbates the Risk of Intracranial Aneurysms.Brain and behavior · 2026Article
- Metabolic Mechanisms in Electroconvulsive Therapy for Schizophrenia: Role, Potential and Future Directions.International journal of molecular sciences · 2026Review
- Identifying established human placental markers of schizophrenia in rodents after gestational ∆9-tetrahydrocannabinol exposure†.Biology of reproduction · 2026Article
- The role of placental DNA methylation in the pathogenesis of chronic intervillositis of unknown etiology.Clinical epigenetics · 2025Article
- Function of epigenetic modifications in wound healing and potential therapies (Review).International journal of molecular medicine · 2025Review
- Impact of placental and peripheral blood DNA methylation on celiac disease susceptibility.Journal of pediatric gastroenterology and nutrition · 2025Article
- Placental DNA methylation key topics: sex- and cell-type specificity, mediation, multi-omics, and biomarker discovery.Epigenomics · 2025Review
- From Womb to Mind: Prenatal Epigenetic Influences on Mental Health Disorders.International journal of molecular sciences · 2025Review
- Saliva as a potential diagnostic medium: DNA methylation biomarkers for disorders beyond the oral cavity.NPJ genomic medicine · 2025Article
- Potentially causal associations between placental DNA methylation and schizophrenia and other neuropsychiatric disorders.Nature communications · 2025Article
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Abstract
Increasing evidence supports the role of the placenta in neurodevelopment and in the onset of neuropsychiatric disorders. Recently, mQTL and iQTL maps have proven useful in understanding relationships between SNPs and GWAS that are not captured by eQTL. In this context, we propose that part of the genetic predisposition to complex neuropsychiatric disorders acts through placental DNA methylation. We construct a public placental cis-mQTL database including 214,830 CpG sites calculated in 368 fetal placenta DNA samples from the INMA project, and run cell type-, gestational age- and sex-imQTL models. We combine these data with summary statistics of GWAS on ten neuropsychiatric disorders using summary-based Mendelian randomization and colocalization. We also evaluate the influence of identified DNA methylation sites on placental gene expression in the RICHS cohort. We find that placental cis-mQTLs are enriched in placenta-specific active chromatin regions, and establish that part of the genetic burden for schizophrenia, bipolar disorder, and major depressive disorder confers risk through placental DNA methylation. The potential causality of several of the observed associations is reinforced by secondary association signals identified in conditional analyses, the involvement of cell type-imQTLs, and the correlation of identified DNA methylation sites with the expression levels of relevant genes in the placenta.
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