ReviewMolecular psychiatry2020
Glycobiology and schizophrenia: a biological hypothesis emerging from genomic research.
Review in Molecular psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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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
45 citing papers in PubMed.
- Beyond the sugar coating: mucin-type O-Glycosylation as an underappreciated player in brain function and disease.Molecular psychiatry · 2026Review
- The ligand preference of LRP1 is regulated by O-glycans.Science advances · 2026Article
- Unraveling the enigma: Post-translational modifications in psychiatric disorders and their regulatory mechanisms.Journal of translational internal medicine · 2026Article
- Stage-Associated Cellular and Molecular Signatures in Diabetic Retinopathy Identified Through Integrated Bulk and Single-Cell Transcriptomic Analysis.International journal of molecular sciences · 2026Article
- GalNAc-T13 maintains neurite architecture and memory retention via O-GalNAc glycosylation of seizure protein 6.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Disrupted O-GalNAc glycosylation as a mechanism and biomarker ofbioRxiv : the preprint server for biology · 2026Article
- Porphyromonas gingivalis-derived outer membrane vesicles promote vascular endothelial glycocalyx injury via the PPAD/CitH3/B3GAT1 pathway.Journal of nanobiotechnology · 2026Article
- Review
- Immunological drivers and potential novel drug targets for major psychiatric, neurodevelopmental, and neurodegenerative conditions.Molecular psychiatry · 2025Article
- Investigating the shared genetic architecture between schizophrenia and sex hormone traits.Translational psychiatry · 2025Article
- O-GalNAc glycans are enriched in neuronal tracts and regulate nodes of Ranvier.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Machine learning identification of molecular targets for medulloblastoma subgroups using microarray gene fingerprint analysis.Computational and structural biotechnology journal · 2025Article
- Investigation of Genetic Changes in Three Families with Bipolar Disease.Molecular syndromology · 2024Article
- The restricted N-glycome of neurons is programmed during differentiation.bioRxiv : the preprint server for biology · 2024Article
- Prognostic value ofHeliyon · 2024Article
- Article
- Clinical glycoproteomics: methods and diseases.MedComm · 2024Review
- Evolutionary conservation of putative suicidality-related risk genes that produce diminished motivation corrected by clozapine, lithium and antidepressants.Frontiers in psychiatry · 2024Article
- Aberrant glycosylation in schizophrenia: insights into pathophysiological mechanisms and therapeutic potentials.Frontiers in pharmacology · 2024Review
- The Correlation Between Peripheral Blood Micro-Ribonucleic Acid Expression Level and Personality Disorder in Patients with Schizophrenia.Alpha psychiatry · 2024Article
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6 authors.
Funding
Abstract
Advances in genomics are opening new windows into the biology of schizophrenia. Though common variants individually have small effects on disease risk, GWAS provide a powerful opportunity to explore pathways and mechanisms contributing to pathophysiology. Here, we highlight an underappreciated biological theme emerging from GWAS: the role of glycosylation in schizophrenia. The strongest coding variant in schizophrenia GWAS is a missense mutation in the manganese transporter SLC39A8, which is associated with altered glycosylation patterns in humans. Furthermore, variants near several genes encoding glycosylation enzymes are unambiguously associated with schizophrenia: FUT9, MAN2A1, TMTC1, GALNT10, and B3GAT1. Here, we summarize the known biological functions, target substrates, and expression patterns of these enzymes as a primer for future studies. We also highlight a subset of schizophrenia-associated proteins critically modified by glycosylation including glutamate receptors, voltage-gated calcium channels, the dopamine D2 receptor, and complement glycoproteins. We hypothesize that common genetic variants alter brain glycosylation and play a fundamental role in the development of schizophrenia. Leveraging these findings will advance our mechanistic understanding of disease and may provide novel avenues for treatment development.
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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.