ArticleNature neuroscience2025
The neuronal chromatin landscape in brains from individuals with schizophrenia is linked to early fetal development.
Article in Nature neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- Memory encoding reprograms neuronal transcriptional responses via durable chromatin remodeling.bioRxiv : the preprint server for biology · 2026Article
- Downregulated transcription in chromosomal domains of midbrain dopamine neurons linked to schizophrenia.Nature communications · 2026Article
- Sex Differences in Brain Cell Type-Specific Chromatin Accessibility in Schizophrenia.Biological psychiatry · 2026Article
- Functional implications of polygenic risk for schizophrenia in human neurons.Nature communications · 2026Article
- Chromatin accessibility provides a window into the genetic etiology of human brain disease.Trends in genetics : TIG · 2025Review
- From compartments to loops: understanding the unique chromatin organization in neuronal cells.Epigenetics & chromatin · 2024Review
- Sex differences in brain cell-type specific chromatin accessibility in schizophrenia.Research square · 2024Article
Corrections and comments
- Update of
- Update of
Authors and funding
21 authors.
Funding
Abstract
Noncoding variants increase neuropsychiatric disease risk, but our understanding of their cell-type-specific role remains incomplete. We conducted large-scale chromatin accessibility profiling of neurons and non-neurons from 2 neocortical regions in 1,393 libraries. We observed substantial differences in neuronal chromatin accessibility between schizophrenia (SCZ) cases and controls, with upregulated open chromatin regions (OCRs) in neurons associated with SCZ risk loci. A comparison of SCZ-associated OCRs with fetal brain-specific OCRs revealed a strong correlation between upregulated changes in SCZ chromatin and openness in fetal cortical brains, linking disease-related chromatin alterations to neurodevelopment. Here we show that a prominent neuronal trans-regulatory domain containing upregulated OCRs consolidates key neurodevelopmental chromatin signatures and is enriched for immature glutamatergic neurons. These findings link altered adult cortical chromatin states to early developmental mechanisms in SCZ. This study provides a comprehensive cell-type-resolved chromatin accessibility resource for the human cortex and offers insights into the regulatory architecture underlying SCZ risk.
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.