ArticleNeurobiology of disease2023
Epigenomic analysis of Alzheimer's disease brains reveals diminished CTCF binding on genes involved in synaptic organization.
Article in Neurobiology of disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 24 citations in OpenAlex.
- Epigenetic regulators polyphenols in neurodegenerative diseases: a promising intervention strategy.Annals of medicine · 2026Review
- DeCTCF: Decoding CTCF binding sequences by leveraging predicted epigenomic features.PLoS computational biology · 2026Article
- Functional Annotation of Alzheimer's Disease-Associated SNPs Based on Three-Dimensional Chromatin Structure.International journal of molecular sciences · 2026Article
- From viral epigenetic reprogramming to neuroinflammation: Mechanisms driving neurodegeneration.Journal of neurovirology · 2026Review
- Sex-biased intron retention in Alzheimer's disease.Neural regeneration research · 2026Article
- Omics-driven strategies for identifying biomarkers in Alzheimer's disease.Metabolic brain disease · 2026Review
- DNA methylation signatures of treatment response in medication-overuse headache.The journal of headache and pain · 2026Observational
- HMGCS2-dependent β-OHB/H3K9bhb ameliorates synaptic plasticity and cognition in Alzheimer's disease.Experimental & molecular medicine · 2026Article
- Conserved 3D genome reorganization during DNA repair.Life science alliance · 2026Review
- Blood gene expression network expression strongly relates to brain amyloid burden.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- CTCF-RNA interactions orchestrate cell-specific chromatin loop organization.Science advances · 2025Article
- Causal Effects of the Plasma Proteome on Vascular Dementia Risk: A Mendelian Randomization Study with Experimental Validation.Cellular and molecular neurobiology · 2025Article
- Identifying deleterious noncoding variation through gain and loss of CTCF binding activity.American journal of human genetics · 2025Article
- Differential Transcriptional Programs Reveal Modular Network Rearrangements Associated with Late-Onset Alzheimer's Disease.International journal of molecular sciences · 2025Article
- Higher Intron Retention Levels in Female Alzheimer's Brains May Be Linked to Disease Prevalence.Aging cell · 2025Article
- Gaining insights into Alzheimer's disease by predicting chromatin spatial organization.Bioinformatics advances · 2025Article
- Article
- The impact of sex on memory during aging and Alzheimer's disease progression: Epigenetic mechanisms.Journal of Alzheimer's disease : JAD · 2024Review
- The chromatin tapestry as a framework for neurodevelopment.Genome research · 2024Review
- Unlocking the epigenetic symphony: histone acetylation's impact on neurobehavioral change in neurodegenerative disorders.Epigenomics · 2024Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Epigenetic aberrations are suggested to play an important role in transcriptional alterations in Alzheimer's disease (AD). One of the key mechanisms of epigenetic regulation of gene expression is through the dynamic organization of chromatin structure via the master genome architecture protein, CCCTC-binding factor (CTCF). By forming chromatin loops, CTCF can influence gene transcription in a complex manner. To find out whether genome-wide DNA binding sites for CTCF are altered in AD, we compared CTCF chromatin immunoprecipitation sequencing (ChIP-Seq) data from frontal cortex of human AD patients and normal controls (n = 9 pairs, all females). We have revealed that CTCF-binding affinity on many genes is significantly reduced in AD patients, and these genes are enriched in synaptic organization, cell adhesion, and actin cytoskeleton, including synaptic scaffolding molecules and receptors, such as SHANK2, HOMER1, NRXN1, CNTNAP2 and GRIN2A, and protocadherin (PCDH) and cadherin (CDH) family members. By comparing transcriptomic data from AD patients, we have discovered that many of the synaptic and adhesion genes with reduced CTCF binding in AD are significantly reduced in their mRNA expression. Moreover, a significant overlap of genes with the diminished CTCF binding and the reduced H3K27ac is identified in AD, with the common genes enriched in synaptic organization. These data suggest that the CTCF-controlled 3D chromatin organization is perturbed in AD, which may be linked to the diminished expression of target genes, probably through changes in histone modification.
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