ArticleGeroScience2022
Brain cellular senescence in mouse models of Alzheimer's disease.
Article in GeroScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 30 citations in OpenAlex.
- Cell Type-Specific Expression of p16, p21, and p53 Reveals Age-Dependent Glial Senescence in the AppAging cell · 2026Article
- Review
- Senotherapeutics for Brain Aging Management.Neurology international · 2025Review
- Senolytics as Modulators of Critical Signaling Pathways: a Promising Strategy to Combat Brain Aging and Neurodegenerative Disorders.Molecular neurobiology · 2025Review
- 27-Hydroxycholesterol triggers microglial senescence subsequent to iron over-loading contributes to brain aging, suppressed by Deferoxamine.npj aging · 2025Article
- Hypoxic Natural Killer Cells-Derived HIF-1α-Containing Exosomes Inhibit Cellular Senescence and Apoptosis in Neurocytes to Ameliorate Alzheimer's Disease by Eliminating Oxidative Damages.Molecular neurobiology · 2025Article
- Entwined processes in Alzheimer's disease: Brain cellular senescence and Alzheimer's disease pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Connections Between Cellular Senescence and Alzheimer's Disease-A Narrative Review.International journal of molecular sciences · 2025Review
- Construction of epilepsy diagnosis model based on cell senescence-related genes and its potential mechanism.Frontiers in neurology · 2025Article
- The role of cellular senescence in neurodegenerative diseases.Archives of toxicology · 2024Review
- Irisin inhibits microglial senescence via TFAM-mediated mitochondrial metabolism in a mouse model of tauopathy.Immunity & ageing : I & A · 2024Article
- Article
- Exploring the Influence of Gut-Brain Axis Modulation on Cognitive Health: A Comprehensive Review of Prebiotics, Probiotics, and Symbiotics.Nutrients · 2024Review
- Endothelial deficiency of insulin-like growth factor-1 receptor leads to blood-brain barrier disruption and accelerated endothelial senescence in mice, mimicking aspects of the brain aging phenotype.Microcirculation (New York, N.Y. : 1994) · 2024Article
- Geroscience and pathology: a new frontier in understanding age-related diseases.Pathology oncology research : POR · 2024Review
- Senescence Targeting Methods Impact Alzheimer's Disease Features in 3xTg Mice.Journal of Alzheimer's disease : JAD · 2024Article
- A Need for Refined Senescence Biomarkers and Measures of Senolytics in the Brain.Journal of Alzheimer's disease : JAD · 2024Article
- The Role of Methionine-Rich Diet in Unhealthy Cerebrovascular and Brain Aging: Mechanisms and Implications for Cognitive Impairment.Nutrients · 2023Review
- Redox-Mediated Rewiring of Signalling Pathways: The Role of a Cellular Clock in Brain Health and Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Neuromodulatory effect of vardenafil on aluminium chloride/D-galactose induced Alzheimer's disease in rats: emphasis on amyloid-beta, p-tau, PI3K/Akt/p53 pathway, endoplasmic reticulum stress, and cellular senescence.Inflammopharmacology · 2023Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The accumulation of senescent cells contributes to aging pathologies, including neurodegenerative diseases, and its selective removal improves physiological and cognitive function in wild-type mice as well as in Alzheimer's disease (AD) models. AD models recapitulate some, but not all components of disease and do so at different rates. Whether brain cellular senescence is recapitulated in some or all AD models and whether the emergence of cellular senescence in AD mouse models occurs before or after the expected onset of AD-like cognitive deficits in these models are not yet known. The goal of this study was to identify mouse models of AD and AD-related dementias that develop measurable markers of cellular senescence in brain and thus may be useful to study the role of cellular senescence in these conditions. We measured the levels of cellular senescence markers in the brains of P301S(PS19), P301L, hTau, and 3xTg-AD mice that model amyloidopathy and/or tauopathy in AD and related dementias and in wild-type, age-matched control mice for each strain. Expression of cellular senescence markers in brains of transgenic P301L and 3xTg-AD mice was largely indistinguishable from that in WT control age-matched mice. In contrast, markers of cellular senescence were differentially increased in brains of transgenic hTau and P301S(PS19) mice as compared to WT control mice before the onset of AD-like cognitive deficits. Taken together, our data suggest that P301S(PS19) and hTau mice may be useful models for the study of brain cellular senescence in tauopathies including, but not limited to, 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.