ReviewActa neuropathologica communications2023
The contribution of DNA methylation to the (dys)function of oligodendroglia in neurodegeneration.
Review in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Role of Hydrogen Sulfide (HInternational journal of molecular sciences · 2023Pooled it
- Early oligodendrocyte dysfunction signature in Alzheimer's disease: Insights from DNA methylomics and transcriptomics.Molecular psychiatry · 2026Article
- An epigenetic clock for chronological age estimation in East Asian populations.NAR genomics and bioinformatics · 2026Article
- Epigenetic mechanisms of inflammatory memory in the central nervous system.Nature immunology · 2026Review
- CpGene: a web application for epigenetic signature identification from DNA methylation arrays.Bioinformatics (Oxford, England) · 2026Article
- Cross-disease genetic and epigenetic architecture of thebioRxiv : the preprint server for biology · 2026Article
- Review
- Integrative epigenomic landscape of Alzheimer's Disease brains reveals oligodendrocyte molecular perturbations associated with tau.Nature communications · 2026Article
- DNA methylation as a contributor to dysregulation of STX6 and other frontotemporal Lobar degeneration genetic risk-associated loci.Acta neuropathologica communications · 2025Article
- DNA methylation as a contributor to dysregulation ofbioRxiv : the preprint server for biology · 2025Article
- Epigenetics factors in schizophrenia: future directions for etiologic and therapeutic study approaches.Annals of general psychiatry · 2025Review
- Article
- DNA methylation patterns in the frontal lobe white matter of multiple system atrophy, Parkinson's disease, and progressive supranuclear palsy: a cross-comparative investigation.Acta neuropathologica · 2024Article
- An Epigenetic Manifestation of Alzheimer's Disease: DNA Methylation.Actas espanolas de psiquiatria · 2024Review
- Distinctive cell-free DNA methylation characterizes presymptomatic genetic frontotemporal dementia.Annals of clinical and translational neurology · 2024Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Neurodegenerative diseases encompass a heterogeneous group of conditions characterised by the progressive degeneration of the structure and function of the central or peripheral nervous systems. The pathogenic mechanisms underlying these diseases are not fully understood. However, a central feature consists of regional aggregation of proteins in the brain, such as the accumulation of β-amyloid plaques in Alzheimer's disease (AD), inclusions of hyperphosphorylated microtubule-binding tau in AD and other tauopathies, or inclusions containing α-synuclein in Parkinson's disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA). Various pathogenic mechanisms are thought to contribute to disease, and an increasing number of studies implicate dysfunction of oligodendrocytes (the myelin producing cells of the central nervous system) and myelin loss. Aberrant DNA methylation, the most widely studied epigenetic modification, has been associated with many neurodegenerative diseases, including AD, PD, DLB and MSA, and recent findings highlight aberrant DNA methylation in oligodendrocyte/myelin-related genes. Here we briefly review the evidence showing that changes to oligodendrocytes and myelin are key in neurodegeneration, and explore the relevance of DNA methylation in oligodendrocyte (dys)function. As DNA methylation is reversible, elucidating its involvement in pathogenic mechanisms of neurodegenerative diseases and in dysfunction of specific cell-types such as oligodendrocytes may bring opportunities for therapeutic interventions for these diseases.
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