ArticleFrontiers in neuroscience2025
Expression and potential regulatory mechanism of cellular senescence-related genes in Alzheimer's disease based on single-cell and bulk RNA datasets.
Article in Frontiers in neuroscience, 2025. 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.
- High mobility group box 1 and its post-translational modifications: Molecular mechanisms underlying neurodegenerative disease pathogenesis.Neural regeneration research · 2026Article
- Review
- Regional astrocyte dysregulation and altered glymphatic-related markers in Alzheimer's disease frontal cortex.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Article
- Single-Nucleus Profiling Reveals a BBB Senescence Unit Driving AD Pathology in Human Brain.Molecular neurobiology · 2026Article
- A conceptual model of oxygen-ozone therapy as a modulator of aging via the HMGB1 pathway.Biogerontology · 2025Review
- Senotherapeutics for Brain Aging Management.Neurology international · 2025Review
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Authors and funding
6 authors.
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Abstract
Introduction: Alzheimer's disease (AD) is the most common cause of dementia in the elderly. However, the particular cause of AD development has not been fully elucidated. Currently, cellular senescence is recognized as a contributing factor to the aging process and age-related diseases. Methods: The present study aimed to identify the hinge of regulatory factors in dysfunctional cellular senescence genes in AD via integrating multiple omics analysis, including single-cell RNA sequencing and bulk sequencing data. In addition, UMAP scatter diagrams were constructed, while active cell subtypes and pathways involved in cellular senescence were identified via performing Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, respectively. Results: The results indicated that a total of seven clusters were detected by known marker genes, including excitatory neurons, inhibitory neurons, astrocytes, microglial cells, oligodendrocytes, oligodendrocyte progenitor cells and pericytes/endothelial cells. Conclusion: The above findings demonstrated that cellular senescence could play a crucial role in the pathogenesis of AD and highlighted the significance of understanding the role of cellular senescence in the pathogenesis of AD. The results of the current study could provide novel insights into the development of potential therapeutic targets and pave the way for the development of novel therapeutic strategies for AD.
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