ReviewBiological psychiatry2022
Schizophrenia Genomics: Convergence on Synaptic Development, Adult Synaptic Plasticity, or Both?
Review in Biological psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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.
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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
51 citing papers in PubMed.
- Rethinking schizophrenia: insights from genomics and implications for research.Molecular psychiatry · 2026Review
- Grin2a knockout in adolescent dopamine neurons disrupts prediction error signaling and produces a phenotype relevant to schizophrenia.Molecular psychiatry · 2026Article
- The Molecular Machinery of Synaptic Plasticity and Its Potential Role in the Aetiology of Schizophrenia.Molecular neurobiology · 2026Review
- Review
- The criticome as the window of becoming: Toward a novel and comprehensive framework for understanding the critical period of information integration in human development.Brain health : lifelong brain resilience and longevity · 2026Article
- Methylome-Wide Association Studies of Physical Injury Stratified by Depression Status Assesses Exposure by Diagnosis Effects in Oxytocin Signaling and Synaptic Plasticity.Biological psychiatry global open science · 2026Article
- Autophagy in Schizophrenia: A Continuum From Developmental Vulnerability to Progressive Neuronal Stress? A Scoping Review.Schizophrenia bulletin · 2026Article
- Natural selection and language genes in humans.Scientific reports · 2026Article
- Protein-protein interaction-interfering peptide rescues dysregulated NMDA receptor signaling.JCI insight · 2026Article
- Integrative Multiomics Analysis Identifies DKK3 as a Germline Susceptibility-Related Regulator of Risperidone Response and Metabolic Risk in Schizophrenia.Human mutation · 2026Article
- Polyunsaturated fatty acids and psychotic disorders: integrating mechanistic, genetic, and clinical evidence.Frontiers in nutrition · 2026Review
- Hemispheric Asymmetry in the Genetic Overlap between Schizophrenia and White Matter Microstructure.Cyborg and bionic systems (Washington, D.C.) · 2026Article
- Cell-type-specific DNA methylation dynamics in the prenatal and postnatal human cortex.Cell genomics · 2025Article
- IncreasingBiological psychiatry global open science · 2025Article
- Glutamate, Contextual Insensitivity, and Disorganized Speech in First-Episode Schizophrenia: A 7T Magnetic Resonance Spectroscopy Study.Biological psychiatry global open science · 2025Article
- CNPI: Rapid Analyses of Human Copy Number Data.Journal of molecular biology · 2025Article
- Obstetric complications, cortical gyrification, and cognition in first-episode psychosis.Psychological medicine · 2025Article
- Rare Copy Number Variants Reveal Critical Cell Types and Periods of Brain Development in Neurodevelopmental Disorders.Biological psychiatry global open science · 2025Article
- The Role of Astrocytes in the Molecular Pathophysiology of Schizophrenia: Between Neurodevelopment and Neurodegeneration.Biomolecules · 2025Review
- A Genome-Wide Association Study of First-Episode Psychosis: A Genetic Exploration in an Italian Cohort.Genes · 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
2 authors.
Funding
Abstract
Large-scale genomic studies of schizophrenia have identified hundreds of genetic loci conferring risk to the disorder. This progress offers an important route toward defining the biological basis of the condition and potentially developing new treatments. In this review, we discuss insights from recent genome-wide association study, copy number variant, and exome sequencing analyses of schizophrenia, together with functional genomics data from the pre- and postnatal brain, in relation to synaptic development and function. These data provide strong support for the view that synaptic dysfunction within glutamatergic and GABAergic (gamma-aminobutyric acidergic) neurons of the cerebral cortex, hippocampus, and other limbic structures is a central component of schizophrenia pathophysiology. Implicated genes and functional genomic data suggest that disturbances in synaptic connectivity associated with susceptibility to schizophrenia begin in utero but continue throughout development, with some alleles conferring risk to the disorder through direct effects on synaptic function in adulthood. This model implies that novel interventions for schizophrenia could include broad preventive approaches aimed at enhancing synaptic health during development as well as more targeted treatments aimed at correcting synaptic function in affected adults.
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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.