ArticleNature communications2021
Neuronal and glial 3D chromatin architecture informs the cellular etiology of brain disorders.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis 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
69 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
- Genetic insights into human cortical organization and development through genome-wide analyses of 2,347 neuroimaging phenotypes.Nature genetics · 2023Pooled it
- Review
- Massively parallel assessment of gene regulatory activity at human cortical-structure-associated variants.Nature neuroscience · 2026Article
- Characterization of the chromosome 7 locus associated with suicidal behavior.Molecular psychiatry · 2026Article
- miR155, triplicated in Down syndrome, regulates the development of neural stem cells and GABAergic interneurons in Alzheimer's disease mouse and human iPSC models.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Long-read transcriptomics of purified human cortical cell types exposes glial isoform complexity and disease-relevant transcript architecture.bioRxiv : the preprint server for biology · 2026Article
- MECP2 mutations disrupt pluripotent stem cell fate through remodeling of the three-dimensional genome.Cell death & disease · 2026Article
- 3D genetic architecture of schizophrenia risk across three neuronal subtypes.Molecular psychiatry · 2026Article
- Microfluidic low-input profiling reveals lncRNA roles in disease.bioRxiv : the preprint server for biology · 2026Article
- Schizophrenia risk variants modulate transcription factor binding and gene expression in cortical cell types.Cellular and molecular life sciences : CMLS · 2026Article
- Repeat expansions inbioRxiv : the preprint server for biology · 2026Article
- Neurogenesis and the Epigenetic Landscape: Role of Histone Modifications and Chromatin Remodeling.Brain and behavior · 2026Review
- A developmentally regulated long-range enhancer-promoter contact mediates human neural development.bioRxiv : the preprint server for biology · 2026Article
- Functional implications of polygenic risk for schizophrenia in human neurons.Nature communications · 2026Article
- Sex-specific role of the 5-HTNature communications · 2025Article
- The inner nuclear membrane protein LEMD3 organizes the 3D chromatin architecture to maintain vascular smooth muscle cell identity.Nature communications · 2025Article
- Dynamic changes in chromosome and nuclear architecture during maturation of normal and ALS C9orf72 motor neurons.bioRxiv : the preprint server for biology · 2025Article
- Single-nucleus chromatin accessibility profiling identifies cell types and functional variants contributing to major depression.Nature genetics · 2025Article
- Analysis of biased allelic enhancer activity of schizophrenia-linked common variants.Communications biology · 2025Article
- Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 20 institutions in 3 countries.
Funding
Abstract
Cellular heterogeneity in the human brain obscures the identification of robust cellular regulatory networks, which is necessary to understand the function of non-coding elements and the impact of non-coding genetic variation. Here we integrate genome-wide chromosome conformation data from purified neurons and glia with transcriptomic and enhancer profiles, to characterize the gene regulatory landscape of two major cell classes in the human brain. We then leverage cell-type-specific regulatory landscapes to gain insight into the cellular etiology of several brain disorders. We find that Alzheimer's disease (AD)-associated epigenetic dysregulation is linked to neurons and oligodendrocytes, whereas genetic risk factors for AD highlighted microglia, suggesting that different cell types may contribute to disease risk, via different mechanisms. Moreover, integration of glutamatergic and GABAergic regulatory maps with genetic risk factors for schizophrenia (SCZ) and bipolar disorder (BD) identifies shared (parvalbumin-expressing interneurons) and distinct cellular etiologies (upper layer neurons for BD, and deeper layer projection neurons for SCZ). Collectively, these findings shed new light on cell-type-specific gene regulatory networks in brain disorders.
Indexed as
Identifiers
What 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.