ArticleMolecular neurodegeneration2021
Sex dependent glial-specific changes in the chromatin accessibility landscape in late-onset Alzheimer's disease brains.
Article in Molecular neurodegeneration, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Cellular transcriptomic signatures underpinning the heterogeneity of depression in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Chromatin accessibility provides a window into the genetic etiology of human brain disease.Trends in genetics : TIG · 2025Review
- Integrative single-nucleus multi-omics analysis prioritizes candidate cis and trans regulatory networks and their target genes in Alzheimer's disease brains.Cell & bioscience · 2023Article
- In-depth proteome analysis of brain tissue from Ewsr1 knockout mouse by multiplexed isobaric tandem mass tag labeling.Scientific reports · 2023Article
- Differential Gene Expression and DNA Methylation in the Risk of Depression in LOAD Patients.Biomolecules · 2022Article
- The three-dimensional landscape of cortical chromatin accessibility in Alzheimer's disease.Nature neuroscience · 2022Article
- Factors Influencing Alzheimer's Disease Risk: Whether and How They are Related to the APOE Genotype.Neuroscience bulletin · 2022Review
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
backgroundIn the post-GWAS era, there is an unmet need to decode the underpinning genetic etiologies of late-onset Alzheimer's disease (LOAD) and translate the associations to causation.
methodsWe conducted ATAC-seq profiling using NeuN sorted-nuclei from 40 frozen brain tissues to determine LOAD-specific changes in chromatin accessibility landscape in a cell-type specific manner.
resultsWe identified 211 LOAD-specific differential chromatin accessibility sites in neuronal-nuclei, four of which overlapped with LOAD-GWAS regions (±100 kb of SNP). While the non-neuronal nuclei did not show LOAD-specific differences, stratification by sex identified 842 LOAD-specific chromatin accessibility sites in females. Seven of these sex-dependent sites in the non-neuronal samples overlapped LOAD-GWAS regions including APOE. LOAD loci were functionally validated using single-nuclei RNA-seq datasets.
conclusionsUsing brain sorted-nuclei enabled the identification of sex-dependent cell type-specific LOAD alterations in chromatin structure. These findings enhance the interpretation of LOAD-GWAS discoveries, provide potential pathomechanisms, and suggest novel LOAD-loci.
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