ReviewSchizophrenia research2020
The three-dimensional landscape of the genome in human brain tissue unveils regulatory mechanisms leading to schizophrenia risk.
Review in Schizophrenia research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis 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
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Common genetic risk variants identified in the SPARK cohort support DDHD2 as a candidate risk gene for autism.Translational psychiatry · 2020Pooled it
- Perturbation of genes linked to common schizophrenia risk variants identifies cilia programs.bioRxiv : the preprint server for biology · 2026Article
- Analysis of biased allelic enhancer activity of schizophrenia-linked common variants.Communications biology · 2025Article
- Article
- Identification of Schizophrenia-Risk Regulatory Variant rs1399178 in the Non-coding Region With Its Impact on NRF1 Binding.CNS neuroscience & therapeutics · 2025Article
- Unraveling the three-dimensional (3D) genome architecture in Neurodevelopmental Disorders (NDDs).Neurogenetics · 2024Review
- Systematic investigation of allelic regulatory activity of schizophrenia-associated common variants.Cell genomics · 2023Article
- Illuminating links between cis-regulators and trans-acting variants in the human prefrontal cortex.Genome medicine · 2022Article
- Focus on your locus with a massively parallel reporter assay.Journal of neurodevelopmental disorders · 2022Review
- Chromatin architecture in addiction circuitry identifies risk genes and potential biological mechanisms underlying cigarette smoking and alcohol use traits.Molecular psychiatry · 2022Article
- Endosomal trafficking in schizophrenia.Current opinion in neurobiology · 2022Review
- Regulatory variants at 2q33.1 confer schizophrenia risk by modulating distal gene TYW5 expression.Brain : a journal of neurology · 2022Article
- Advances in profiling chromatin architecture shed light on the regulatory dynamics underlying brain disorders.Seminars in cell & developmental biology · 2022Review
- Schizophrenia-Linked Protein tSNARE1 Regulates Endosomal Trafficking in Cortical Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Limited Association between Schizophrenia Genetic Risk Factors and Transcriptomic Features.Genes · 2021Article
- Chromatin architecture provides a roadmap to improve our understanding of psychiatric disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- Parsing the Functional Impact of Noncoding Genetic Variants in the Brain Epigenome.Biological psychiatry · 2021Review
- Regulatory landscape in brain development and disease.Current opinion in genetics & development · 2020Review
- A chromosomal connectome for psychiatric and metabolic risk variants in adult dopaminergic neurons.Genome medicine · 2020Article
- Mapping Alzheimer's Disease Variants to Their Target Genes Using Computational Analysis of Chromatin Configuration.Journal of visualized experiments : JoVE · 2020Article
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 at 1 institution in 1 country.
Funding
Abstract
Recent advances in our understanding of the genetic architecture of schizophrenia have shed light on the schizophrenia etiology. While common variation is one of the major genetic contributors, the majority of common variation reside in non-coding genome, posing a significant challenge in understanding the functional impact of this class of genetic variation. Functional genomic datasets that range from expression quantitative trait loci (eQTL) to chromatin interactions are critical to identify the potential target genes and functional consequences of non-coding variation. In this review, we discuss how three-dimensional chromatin landscape, identified by a technique called Hi-C, has facilitated the identification of potential target genes impacting schizophrenia risk. We outline key steps for Hi-C driven gene mapping, and compare Hi-C defined schizophrenia risk genes defined across developmental epochs and cell types, which offer rich insights into the temporal window and cellular etiology of schizophrenia. In contrast with a neurodevelopmental hypothesis in schizophrenia, Hi-C defined schizophrenia risk genes are postnatally enriched, suggesting that postnatal development is also important for schizophrenia pathogenesis. Moreover, Hi-C defined schizophrenia risk genes are highly expressed in excitatory neurons, highlighting excitatory neurons as a central cell type for schizophrenia. Further characterization of Hi-C defined schizophrenia risk genes demonstrated enrichment for genes that harbor loss-of-function variation in neurodevelopmental disorders, suggesting a shared genetic etiology between schizophrenia and neurodevelopmental disorders. Collectively, moving the search space from risk variants to the target genes lays a foundation to understand the neurobiological basis of schizophrenia.
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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.