ArticleNature neuroscience2018
Cell-specific histone modification maps in the human frontal lobe link schizophrenia risk to the neuronal epigenome.
Article in Nature neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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
82 citing papers in PubMed, 154 citations in OpenAlex.
- Article
- Characterization of the chromosome 7 locus associated with suicidal behavior.Molecular psychiatry · 2026Article
- Analysis of gene co-expression connectivity dynamics implicates aberrant neuron-oligodendroglia interactions in schizophrenia.Nature communications · 2026Article
- Histone Modifications in Psychiatry: From Canonical Marks to Neurotransmitter-Mediated Epigenetic Signatures.Alpha psychiatry · 2026Review
- Sex Differences in Brain Cell Type-Specific Chromatin Accessibility in Schizophrenia.Biological psychiatry · 2026Article
- 3D genetic architecture of schizophrenia risk across three neuronal subtypes.Molecular psychiatry · 2026Article
- Modifications on histone tails in psychiatric disorders.EC psychology and psychiatry · 2026Article
- Exploration of schizophrenia-associated gene modules using graph theory, co-expression networks, and dimensionality reduction.PloS one · 2026Article
- Mutations of schizophrenia risk gene SETD1A dysregulate synaptic function in human neurons.Molecular psychiatry · 2025Article
- Molecular Signatures of Schizophrenia and Insights into Potential Biological Convergence.International journal of molecular sciences · 2025Review
- Single-nucleus chromatin accessibility profiling identifies cell types and functional variants contributing to major depression.Nature genetics · 2025Article
- Population-scale cross-disorder atlas of the human prefrontal cortex at single-cell resolution.Scientific data · 2025Article
- Human brain aging is associated with dysregulation of cell type epigenetic identity.GeroScience · 2025Article
- CHAS infers cell type-specific signatures in bulk brain histone acetylation studies of neurological and psychiatric disorders.Cell reports methods · 2025Article
- Genetic risk for neurodegenerative conditions is linked to disease-specific microglial pathways.PLoS genetics · 2025Article
- The Promise of Epigenetic Editing for Treating Brain Disorders.Sub-cellular biochemistry · 2025Review
- Biomarkers in Schizophrenia: Current Approaches and New Developments-A Literature Review.Behavioural neurology · 2025Review
- Single chromatin fiber profiling and nucleosome position mapping in the human brain.Cell reports methods · 2024Article
- Modeling common and rare genetic risk factors of neuropsychiatric disorders in human induced pluripotent stem cells.Schizophrenia research · 2024Review
- Article
22 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
26 authors at 6 institutions in 2 countries.
Funding
Abstract
Risk variants for schizophrenia affect more than 100 genomic loci, yet cell- and tissue-specific roles underlying disease liability remain poorly characterized. We have generated for two cortical areas implicated in psychosis, the dorsolateral prefrontal cortex and anterior cingulate cortex, 157 reference maps from neuronal, neuron-depleted and bulk tissue chromatin for two histone marks associated with active promoters and enhancers, H3-trimethyl-Lys4 (H3K4me3) and H3-acetyl-Lys27 (H3K27ac). Differences between neuronal and neuron-depleted chromatin states were the major axis of variation in histone modification profiles, followed by substantial variability across subjects and cortical areas. Thousands of significant histone quantitative trait loci were identified in neuronal and neuron-depleted samples. Risk variants for schizophrenia, depressive symptoms and neuroticism were significantly over-represented in neuronal H3K4me3 and H3K27ac landscapes. Our Resource, sponsored by PsychENCODE and CommonMind, highlights the critical role of cell-type-specific signatures at regulatory and disease-associated noncoding sequences in the human frontal lobe.
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.