ArticleCommunications biology2024
Differential methylation analysis in neuropathologically confirmed dementia with Lewy bodies.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- DNA methylation variability provides a complementary epigenetic signature of aging heterogeneity: Findings from the Canadian Longitudinal Study on Aging and the Baltimore Longitudinal Study of Aging.bioRxiv : the preprint server for biology · 2026Article
- Imaging brain class I histone deacetylase changes in the Lewy body dementias and Parkinson's disease.Clinical epigenetics · 2026Article
- Methylomic signatures of tau and amyloid-beta in transgenic mouse models of Alzheimer's disease neuropathology.NPJ dementia · 2026Article
- Cerebellum in Alzheimer's disease and other neurodegenerative diseases: an emerging research frontier.MedComm · 2024Review
Corrections and comments
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Authors and funding
24 authors at 11 institutions in 4 countries.
Funding
Abstract
Dementia with Lewy bodies (DLB) is a common form of dementia in the elderly population. We performed genome-wide DNA methylation mapping of cerebellar tissue from pathologically confirmed DLB cases and controls to study the epigenetic profile of this understudied disease. After quality control filtering, 728,197 CpG-sites in 278 cases and 172 controls were available for the analysis. We undertook an epigenome-wide association study, which found a differential methylation signature in DLB cases. Our analysis identified seven differentially methylated probes and three regions associated with DLB. The most significant CpGs were located in ARSB (cg16086807), LINC00173 (cg18800161), and MGRN1 (cg16250093). Functional enrichment evaluations found widespread epigenetic dysregulation in genes associated with neuron-to-neuron synapse, postsynaptic specialization, postsynaptic density, and CTCF-mediated synaptic plasticity. In conclusion, our study highlights the potential importance of epigenetic alterations in the pathogenesis of DLB and provides insights into the modified genes, regions and pathways that may guide therapeutic developments.
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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.