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Cellular senescence in aging and age-related diseases: Implications for neurodegenerative diseases
Open accessAbstract
Aging is the major predictor for developing multiple neurodegenerative diseases, including Alzheimer's disease (AD) other dementias, and Parkinson's disease (PD). Senescent cells, which can drive aging phenotypes, accumulate at etiological sites of many age-related chronic diseases. These cells are resistant to apoptosis and can cause local and systemic dysfunction. Decreasing senescent cell abundance using senolytic drugs, agents that selectively target these cells, alleviates neurodegenerative diseases in preclinical models. In this review, we consider roles of senescent cells in neurodegenerative diseases and potential implications of senolytic agents as an innovative treatment.
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“Aging progresses throughout the lifespan can be accentuated at etiologic sites of multiple acute and chronic diseases, including in children6,8–12.”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [8]
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“To date, research conducted across six transgenic AD mouse models has demonstrated that orally administered senolytic drugs ablate senescent cells in the brain and alleviate AD-relevant pathogenesis (28–30, 32).”
From Senolytic Therapy to Modulate the Progression of Alzheimer's Disease (SToMP-AD): A Pilot Clinical Trial (2022) · cites this paper as [32]
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“Recent evidence suggests that the accumulation of senescent cells, which can release a variety of pro-inflammatory, apoptotic, and toxic by-products, called the senescence-associated secretory phenotype (SASP), is one of the drivers of deficits in both cognition11, 12, 13, 14, 15, 16 and mobility.7,17, 18, 19, 20, 21, 22”
From A pilot study of senolytics to improve cognition and mobility in older adults at risk for Alzheimer's disease (2025) · cites this paper as [14]
Experimental — accuracy not yet measuredIn the citing paper
“Microglia and astrocytes can acquire a senescent phenotype themselves (28, 31, 32), promoting further diffusion of the SASP and the conversion of healthy cells to the senescent phenotype.”
From Senolytic Therapy to Modulate the Progression of Alzheimer's Disease (SToMP-AD): A Pilot Clinical Trial (2022) · cites this paper as [32]
In the citing paper
“The burden of senescent cells in the brain increases with advanced chronological age and neurodegenerative diseases, and occurs across cell types including neurons, microglia, astrocytes, oligodendrocyte precursor cells, and endothelial cells (28–32).”
From Senolytic Therapy to Modulate the Progression of Alzheimer's Disease (SToMP-AD): A Pilot Clinical Trial (2022) · cites this paper as [32]
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“Collectively, preclinical research has provided strong proof-of-concept data that tau-induced cellular senescence may be a novel therapeutic target for AD (29, 32).”
From Senolytic Therapy to Modulate the Progression of Alzheimer's Disease (SToMP-AD): A Pilot Clinical Trial (2022) · cites this paper as [32]
In the citing paper
“The best characterized senolytic agents are dasatinib (D) plus quercetin (Q) (D+Q) (32).”
From Senolytic Therapy to Modulate the Progression of Alzheimer's Disease (SToMP-AD): A Pilot Clinical Trial (2022) · cites this paper as [32]
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Metadata
- Authors
- Gerdes, E. O. W., Zhu, Y. Z., Weigand, B. M., Tripathi, U., Burns, T. C., Tchkonia, T., & Kirkland, J. L.
- Affiliations
- Mayo Clinic (US)
- Corresponding author
- James L. Kirkland
- Venue
- International Review of Neurobiology
- Publisher
- Elsevier
- Published
- 2020
- Volume
- 155
- Pages
- 203-234
- ISSN
- 0074-7742 (ISSN-L)
- PMC
- PMC7656525
- OpenAlex
- W3048583596
- Cited by
- 114
- References
- 171
- Citations by year
- 2026: 13 · 2025: 25 · 2024: 21 · 2023: 27 · 2022: 16 · 2021: 10
- FWCI
- 54.76
- Type
- book chapter
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- International review of neurobiology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R33AG061456, R37AG013925, P01AG062413)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- cellular senescence, aging, age-related diseases, neurodegenerative diseases, Alzheimer's disease, Parkinson's disease, senolytics, senescent cells, apoptosis resistance, dementia
- MeSH terms
- Aging, Animals, Humans, Cellular Senescence, Neurodegenerative Diseases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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