ReviewNature reviews. Neuroscience2024
Schizophrenia genomics: genetic complexity and functional insights.
Review in Nature reviews. Neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Integrating cell-type-specific gene expression and genome-wide associations identifies risk genes for schizophrenia.Molecular psychiatry · 2026Pooled it
- The relationship among cognitive reserve and symptoms, cognition, and functioning in schizophrenia: A case-control study and meta-analysis.European psychiatry : the journal of the Association of European Psychiatrists · 2026Pooled it
- Does Cannabis Use Contribute to Schizophrenia? A Causation Analysis Based on Epidemiological Evidence.Biomolecules · 2025Pooled it
- Rethinking schizophrenia: insights from genomics and implications for research.Molecular psychiatry · 2026Review
- Genome-wide tandem repeat expansions modify schizophrenia risk in the presence of a 22q11.2 deletion.Molecular psychiatry · 2026Article
- Determinants of functional burden pleiotropy and gene dosage responses across human traits.Nature communications · 2026Article
- The association of schizophrenia polygenic scores with continuously-hospitalized, treatment-resistant schizophrenia.Molecular psychiatry · 2026Article
- Reference Regulatory Element-Guided Gene Expression Analysis for Mechanistic Inference of Gene Regulatory Networks.bioRxiv : the preprint server for biology · 2026Article
- The Cybernetics of Mental Disorders as a Bridge Between Palliative Care and Palliative Psychiatry-A Narrative Review.Healthcare (Basel, Switzerland) · 2026Review
- Developmentally dynamic, non-convergent transcriptomic profiles in CNV models for schizophrenia risk.Molecular psychiatry · 2026Article
- Functional Genomics Studies of Psychiatric Disorders in Individuals of Latin American Populations: A Scoping Review.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2026Article
- Causal inference in psychiatric research: how to critically evaluate and interpret mendelian randomization studies.Molecular psychiatry · 2026Review
- Locus-Specific Genetic Associations at theAdvanced genetics (Hoboken, N.J.) · 2026Article
- Transcription Factors in the Pathogenesis of Schizophrenia.Life (Basel, Switzerland) · 2026Review
- Peripheral lncRNA-IL1RAP Dysregulation in Schizophrenia: A Multi-Omics Bridge Between Immunity and Diagnosis.Brain and behavior · 2026Article
- Mendelian randomization facilitates identification of schizophrenia risk enhancer RNAs.Molecular psychiatry · 2026Article
- Genome-wide fine-mapping improves identification of causal variants.Nature genetics · 2026Article
- Human brain prefrontal cortex proteomics identifies compromised energy metabolism and neuronal function in Schizophrenia.Nature communications · 2026Article
- SN/VTA neuromelanin signal is associated with subclinical paranoia irrespective of familial risk for psychosis.Schizophrenia (Heidelberg, Germany) · 2026Article
- Association ofFrontiers in psychiatry · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Determining the causes of schizophrenia has been a notoriously intractable problem, resistant to a multitude of investigative approaches over centuries. In recent decades, genomic studies have delivered hundreds of robust findings that implicate nearly 300 common genetic variants (via genome-wide association studies) and more than 20 rare variants (via whole-exome sequencing and copy number variant studies) as risk factors for schizophrenia. In parallel, functional genomic and neurobiological studies have provided exceptionally detailed information about the cellular composition of the brain and its interconnections in neurotypical individuals and, increasingly, in those with schizophrenia. Taken together, these results suggest unexpected complexity in the mechanisms that drive schizophrenia, pointing to the involvement of ensembles of genes (polygenicity) rather than single-gene causation. In this Review, we describe what we now know about the genetics of schizophrenia and consider the neurobiological implications of this information.
Indexed as
Identifiers
39030273What OpenQuestion holds
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.