ArticleNature communications2026
Integrative epigenomic landscape of Alzheimer's Disease brains reveals oligodendrocyte molecular perturbations associated with tau.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Early oligodendrocyte dysfunction signature in Alzheimer's disease: Insights from DNA methylomics and transcriptomics.Molecular psychiatry · 2026Article
- Tau Ablation Rewires Brain Cell Programs in Health and Restores Function in Disease.bioRxiv : the preprint server for biology · 2026Article
- AAV-Delivered RNAi Targeting Mutant LDB3 Prevents and Reverses Myofibrillar Myopathy through Mechanosignaling Restoration.bioRxiv : the preprint server for biology · 2026Article
- Brain multiomic profiling identifies tau-related transcriptomic dysregulation in Alzheimer's disease.Brain communications · 2026Article
- Oligodendrocyte dysfunction in neurodegenerative diseases: pathological features, underlying mechanisms and therapeutic targeting.Frontiers in aging neuroscience · 2026Review
- Sphingolipid and ceramide associations with tau pathology vary across diverse ethnoracial groups in postmortem brain tissue.medRxiv : the preprint server for health sciences · 2025Article
- Tau-seed interactome analysis reveals distinct functional signatures in Alzheimer's disease across model systems.bioRxiv : the preprint server for biology · 2025Article
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Abstract
Alzheimer's disease (AD) brains have variable neuropathologic and biochemical changes. Capturing epigenetic factors associated with this variability can reveal novel biological insights into AD pathophysiology. Here, we conduct an epigenome-wide association study of DNA methylation in 472 AD brains with neuropathologic and biochemical brain protein levels core to AD pathogenesis. Using a novel regional methylation (rCpGm) approach, we identify 5478 significant associations, 99.7% of which associate with tau biochemical measures, and 93 concordant associations in external datasets. Transcriptome-methylome integration reveals enrichment in oligodendrocyte genes, including known AD risk gene BIN1, myelination genes MYRF, MBP and MAG previously implicated in AD, and novel genes like LDB3. Further characterization of these perturbations in independent AD and primary tauopathy datasets highlights consistent tau-related associations. In summary, we uncover the integrative epigenomic landscape of AD, demonstrate tau-related oligodendrocyte gene perturbations as a common potential pathomechanism across tauopathies and share findings via our Multiomic Atlas.
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