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 processes can be accentuated at etiologic sites of multiple acute and chronic diseases, including in children.
“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]
The Introduction links cellular senescence to several chronic diseases, and the Brain tumors section says chemoradiation can induce senescence with damaging effects in pediatric patients (page numbers unavailable). The paper also discusses senescence after stroke. These passages support examples of disease- and treatment-associated senescence, but not the broader claim that aging processes are accentuated at the etiologic sites of multiple acute and chronic diseases, including in children. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe introduction argues that senescent cells and their SASP products contribute to deficits in cognition and mobility.
“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 measuredMicroglia and astrocytes can acquire a senescent phenotype, promoting diffusion of the senescence-associated secretory phenotype and conversion of healthy cells to senescence.
“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]
The burden of senescent cells in the brain increases with advanced age and neurodegenerative diseases and occurs across neurons, microglia, astrocytes, oligodendrocyte precursor cells, and endothelial cells.
“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]
Preclinical research provides strong proof-of-concept that tau-induced cellular senescence may be a therapeutic target for Alzheimer's disease.
“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]
Dasatinib plus quercetin are the best characterized senolytic agents.
“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]
Across six transgenic Alzheimer's disease mouse models, orally administered senolytic drugs ablate brain senescent cells and alleviate Alzheimer's-relevant pathogenesis.
“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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TCDD induces UbcH7 expression and synphilin‐1 protein degradation in the mouse ventral midbrain
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Author response: Targeting senescent cells enhances adipogenesis and metabolic function in old age
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Cellular senescence and senolytics: the path to the clinic
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Self-citationNeuroinflammation in Alzheimer’s Disease
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Self-citationThe role of cellular senescence in neurodegenerative diseases
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Orally-active, clinically-translatable senolytics restore α-Klotho in mice and humans
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Self-citationSenolytic Therapy for Cerebral Ischemia-Reperfusion Injury
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“14,27,28 To date, four human studies administering DQ as a combination senolytic therapy have been completed in various populations, including idiopathic pulmonary fi brosis, 29 diabetic kidney disease, 30 age-related osteoporosis, 31 and Alzheimer ’ s disease.”
Self-citationCellular senescence in the aging brain: A promising target for neurodegenerative diseases
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Myelin in Alzheimer’s disease: culprit or bystander?
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SGLT2 Inhibitor Use and Risk of Dementia and Parkinson Disease Among Patients With Type 2 Diabetes
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Biological effects and mechanisms of fisetin in cancer: a promising anti-cancer agent
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Mesenchymal Stromal Cells as a Driver of Inflammaging
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Proteostasis disruption and senescence in Alzheimer’s disease pathways to neurodegeneration
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Neuroinflammaging and the Immune Landscape: The Role of Autophagy and Senescence in Aging Brain
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The Emerging Role of Accelerated Cellular Senescence in Periodontitis
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Self-citationMolecular Mechanisms of Cellular Senescence in Neurodegenerative Diseases
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Tricarboxylic Acid Cycle Intermediates and Individual Ageing
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Effects of Fisetin Treatment on Cellular Senescence of Various Tissues and Organs of Old Sheep
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Senescent Microglia Represent a Subset of Disease-Associated Microglia in P301S Mice
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Senescence and SASP Are Potential Therapeutic Targets for Ischemic Stroke
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Radiation-Induced Macrovessel/Microvessel Disease
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The Health-Promoting Effects and the Mechanism of Intermittent Fasting
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Targeting cIAP2 in a novel senolytic strategy prevents glioblastoma recurrence after radiotherapy
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Tau proteins and senescent Cells: Targeting aging pathways in Alzheimer’s disease
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A Review of ApoE4 Interference Targeting Mitophagy Molecular Pathways for Alzheimer's Disease
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Senolytic treatment fails to improve ovarian reserve or fertility in female mice
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Self-citationMitochondrial and microtubule defects in Exfoliation Glaucoma
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N6-Methyladenosine Methylation of mRNA in Cell Senescence
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Protein kinase inhibitors as therapeutics in neurodegenerative and psychiatric disorders
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Self-citationTargeting senescence and GATA4 in age-related cardiovascular disease: a comprehensive approach
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Report on the Myomatrix Conference April 22–24, 2012, University of Nevada, Reno, Nevada, USA
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A Age Related Vascular Senescence: Mystery of Blood-brain Barrier Dysfunction in Neurodegeneration
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Senescence in Aging, Within the Brain and Other Diseases: Mechanisms and Interventions
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Senotherapeutic approach to age-related endocrine diseases
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Senescence and Beyond: Exploring Senolytic Strategies for Chronic Disease
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TRF2 enriched cytoplasmic chromatin drives cGAS-STAT1-mediated inflammation in senescence
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Self-citationPayea, M. J., Gorospe, M., & Basisty, N. (2022) · Journal of Visualized Experiments · doi:10.3791/63835-v · Cited by 1 · see citing works
Intravenous Uptake of NMN is Safely Metabolize and Increases NAD+ Levels in Healthy SubjectsPreprint
Kimura, S., Ichikawa, M., Sugawara, S., Katagiri, T., Hirasawa, Y., Ishikawa, T., Matsunaga, W., & Gotoh, A. (2022) · Research Square · doi:10.21203/rs.3.rs-1298321/v1 · Cited by 1 · see citing works
The possible biomarkers of the «postСovid-19 syndrome» in patients with type 2 diabetes
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Senescence and its Effect on Aging and Dementia
Khaliq, F. (2022) · Journal of Regenerative Biology and Medicine · doi:10.37191/mapsci-2582-385x-4(3)-114
Fletcher-Sananikone, E., Kanji, S., Tomimatsu, N., Cristofaro, L. F. M. D., Kollipara, R. K., Saha, D., Floyd, J., Sung, P., Hromas, R., Burns, T. C., et al. (2023) · doi:10.1158/0008-5472.c.6513888.v1
Self-citationEffect of DNA damage mediating psychosocial stress on aging
Al-Maeni, M., & Al-Khazraji, S. F. R. (2023) · Iraqi Journal of Cancer and Medical Genetics · doi:10.29409/ijcmg.v16i1.271
Mitochondrial and Microtubule Defects in Exfoliation GlaucomaPreprint
Venkatesan, A., Ridilla, M., Castro, N., Wolosin, J. M., Henty-Ridilla, J. L., Knox, B. E., Ganapathy, P. S., Brown, J. S., DeVincentis, A. F., Sieminski, S. F., et al. (2024) · SSRN Electronic Journal · doi:10.2139/ssrn.5055355
Mitochondrial and Microtubule Defects in Exfoliation GlaucomaPreprint
Venkatesan, A., Ridilla, M., Castro, N., Wolosin, J. M., Henty-Ridilla, J. L., Knox, B. E., Ganapathy, P. S., Brown, J. S., DeVincentis, A. F., Sieminski, S. F., et al. (2025) · SSRN Electronic Journal · doi:10.2139/ssrn.5114437
Cellular Senescence and Lung Diseases: From COPD to Fibrosis
Yadav, V., Bharadwaj, P., & Maruthi, M. (2025) · Springer eBooks · doi:10.1007/978-981-96-1041-9_11
Sun, X., Huang, H., Li, Y., & Jing, F. (2025) · Neurosurgical Review · doi:10.1007/s10143-025-03651-6
Cellular Senescence in Multiple Sclerosis (MS)
Dahiya, R., Dahiya, S., Siddique, R., Thapa, R., Bhat, A. A., Hussain, M. S., Singh, T. G., Singh, S. K., Gupta, S., Deb, P. K., et al. (2025) · Springer eBooks · doi:10.1007/978-981-96-8873-9_11
- 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 · 2015: 1 · 2012: 1
- 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
- Health Sciences › Medicine › Physiology › 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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