SynthesisNature human behaviour2025
Gene-level analysis reveals the genetic aetiology and therapeutic targets of schizophrenia.
Synthesis in Nature human behaviour, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses 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
18 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Integrating cell-type-specific gene expression and genome-wide associations identifies risk genes for schizophrenia.Molecular psychiatry · 2026Pooled it
- Identification of 1q25.2 as a novel shared locus between schizophrenia and major depressive disorder in east Asians by integrative analyses.Translational psychiatry · 2025Pooled it
- Cell-type-specific genetic architecture reveals neuronal and immune contributions to neuropsychiatric disorders.Molecular psychiatry · 2026Article
- Accurate prediction in reconstructed spatial transcriptomes does not ensure valid biological discovery.bioRxiv : the preprint server for biology · 2026Article
- Molecular regulatory mechanisms of schizophrenia-associated functional non-coding variants.Molecular psychiatry · 2026Article
- Proteomic Profiling Captures Residual Cardiovascular Risk Beyond the PREVENT Model in Individuals With Cardiovascular-Kidney-Metabolic Syndrome Stages 2-3.Diabetes, obesity & metabolism · 2026Article
- Evidence for overlapping genetic architecture between lifestyle factors and severe mental disorders with different patterns across diagnoses.EBioMedicine · 2026Article
- Shared genetic architecture of psychiatric disorders and ocular diseases: Evidence from genome-wide analyses.IBRO neuroscience reports · 2026Article
- Genetic and functional insights into long noncoding RNAs in schizophrenia.Molecular psychiatry · 2026Article
- Interpreting artificial neural networks to detect genome-wide association signals for complex traits.NAR genomics and bioinformatics · 2026Article
- Identifying genome-by-childhood trauma interactions for depression using a forest-based approach in the UK Biobank and Adolescent Brain Cognitive Development Study.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Functional variants at 1p36.23 confer risk of schizophrenia through modulating RERE.Nature communications · 2026Article
- Risperidone regulates the expression of schizophrenia-related genes in the forebrain of adult male mice.Frontiers in molecular neuroscience · 2026Article
- Allele-Specific Methylation Links Non-coding Variant of rs2280906 to MYOM2 Regulation in Schizophrenia.Molecular neurobiology · 2025Article
- The regulatory variant rs1950834 confers the risk of depressive disorder by reducing LRFN5 expression.BMC medicine · 2025Article
- Schizophrenia risk gene ZNF536 modulates retinoic acid response and neuronal gene networks in SH-SY5Y cells.Frontiers in molecular neuroscience · 2025Article
- Genetic implication of GABAFrontiers in pharmacology · 2025Review
- HORNET: tools to find genes with causal evidence and their regulatory networks using eQTLs.Bioinformatics advances · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors.
Funding
Abstract
Genome-wide association studies (GWASs) have reported multiple risk loci for schizophrenia (SCZ). However, the majority of the associations were from populations of European ancestry. Here we conducted a large-scale GWAS in Eastern Asian populations (29,519 cases and 44,392 controls) and identified ten Eastern Asian-specific risk loci, two of which have not been previously reported. A further cross-ancestry GWAS meta-analysis (96,806 cases and 492,818 controls) including populations from diverse ancestries identified 61 previously unreported risk loci. Systematic variant-level analysis, including fine mapping, functional genomics and expression quantitative trait loci, prioritized potential causal variants. Gene-level analyses, including transcriptome-wide association study, proteome-wide association study and Mendelian randomization, nominated the potential causal genes. By integrating evidence from layers of different analyses, we prioritized the most plausible causal genes for SCZ, such as ACE, CNNM2, SNAP91, ABCB9 and GATAD2A. Finally, drug repurposing showed that ACE, CA14, MAPK3 and MAPT are potential therapeutic targets for SCZ. Our study not only showed the power of cross-ancestry GWAS in deciphering the genetic aetiology of SCZ, but also uncovered new genetic risk loci, potential causal variants and genes and therapeutic targets for SCZ.
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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.