ReviewJournal of neurochemistry2025
The Role of Glial Cell Senescence in Alzheimer's Disease.
Review in Journal of neurochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed.
- Restores Aβ Clearance by Overcoming PCSK9-LRP1 Dysregulation and TRIB3-Mediated Autophagy Blockade in Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- uPAR exhibits age- and region-dependent expression in the brains of mice with Alzheimer's disease-like pathology.Brain research · 2026Article
- Lithium as a Potential Senostatic Agent in Central Nervous System Aging and Bipolar Disorder.Pharmaceuticals (Basel, Switzerland) · 2026Review
- 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
- Targeting the cGAS-STING pathway alleviates neuroinflammation and cognitive impairment induced by chronic infection of Toxoplasma gondii.Journal of neuroinflammation · 2026Article
- Review
- Aryl Hydrocarbon Receptor Signaling in Aging: A Key Modulator of Brain Homeostasis.Molecular neurobiology · 2026Review
- Single-cell Transcriptomics Reveals that the SORBS1/FBXO22/BAG3 Axis Drives Astrocyte Senescence via Calcium Signaling and Affects Alzheimer's Disease-Related Neuronal Damage.Neuromolecular medicine · 2026Article
- Preface to the Special Issue "Astrocytes in Cognition and Behavior".Journal of neurochemistry · 2026Article
- Beyond biochemical cascades: novel bio-mechanical and epigenetic paradigms of glial SASP in brain aging.Metabolic brain disease · 2026Review
- Dysregulated oligodendrocyte and myelin dynamics as an early pathological feature of neuropil degeneration in Alzheimer's disease: an ultrastructural study.Acta neuropathologica communications · 2026Article
- Viral Mimicry of Alzheimer's Disease: Innate Sensing of Self-Nucleic Acids as a Driver of Glial Senescence.Journal of molecular neuroscience : MN · 2026Review
- SIRT1 Activators as Geroprotective Agents in Brain Aging: Mechanisms and Therapeutic Potential.Neuromolecular medicine · 2026Review
- DNA damage drives a unique, Alzheimer's disease-relevant senescent state in neurons.bioRxiv : the preprint server for biology · 2026Article
- Cellular senescence in brain aging and neurodegeneration: from molecular mechanisms to translational opportunities.Frontiers in cellular neuroscience · 2026Review
- Lipid metabolic regulation of neuroinflammation in Alzheimer's disease.Frontiers in immunology · 2026Review
- Targeting microglia-mediated neuroinflammation in Alzheimer's disease: mechanisms and therapeutic approaches.Frontiers in immunology · 2026Review
- Senotherapeutics for Brain Aging Management.Neurology international · 2025Review
- Research Progress of Lipid Metabolism-Mediated Neuroinflammation in Alzheimer's Disease.Cellular and molecular neurobiology · 2025Review
- Senolytics as Modulators of Critical Signaling Pathways: a Promising Strategy to Combat Brain Aging and Neurodegenerative Disorders.Molecular neurobiology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Glial cell senescence, characterized by the irreversible arrest of cell division and a pro-inflammatory secretory phenotype, has emerged as a critical player in the pathogenesis of Alzheimer's disease (ad). While much attention has been devoted to the role of neurons in ad, growing evidence suggests that glial cells, including astrocytes, microglia, and oligodendrocytes, contribute significantly to disease progression through senescence. In this review, we explore the molecular mechanisms underlying glial cell senescence in ad, focusing on the cellular signaling pathways, including DNA damage response and the accumulation of senescence-associated secretory phenotypes (SASP). We also examine how senescent glial cells exacerbate neuroinflammation, disrupt synaptic function, and promote neuronal death in ad. Moreover, we discuss emerging therapeutic strategies aimed at targeting glial cell senescence to mitigate the neurodegenerative processes in ad. By providing a comprehensive overview of current research on glial cell senescence in Alzheimer's disease, this review highlights its potential as a novel therapeutic target in the fight against ad.
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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.