The DOI matches its Crossref record; 170 of the 171 references it cites were found in a registry or an index.
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]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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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1 retracted
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BackgroundThe serial cultivation of human diploid cell strains
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The senescence-associated secretory phenotype: the dark side of tumor suppression
Coppé, J.-P., Desprez, P.-Y., Krtolica, A., & Campisi, J. (2010) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-121808-102144 · Cited by 5,206
Cellular senescence: when bad things happen to good cells
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Extracellular vesicle-derived mitochondrial genes as potential biomarkers for brain aging in human
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Hai, H., Li, M., Hu, X., Peng, J., & He, Z. (2026) · Frontiers in Neurology · doi:10.3389/fneur.2026.1875385 · Cited by 1
Li, J., Li, Y., Bhat, A., Zheng, M., & Zhang, Q. (2026) · Research Square · doi:10.21203/rs.3.rs-10738655/v1
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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
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