ReviewFrontiers in aging neuroscience2025
Current aspects of targeting cellular senescence for the therapy of neurodegenerative diseases.
Review in Frontiers in aging neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed.
- TLDc proteins: Stress-responsive nexus regulators of redox signaling, V-ATPase dynamics, and organellar crosstalk in neurodegeneration.Redox biology · 2026Review
- Lithium as a Potential Senostatic Agent in Central Nervous System Aging and Bipolar Disorder.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Osteoarthritis and dementia: contrasting disorders driven by mutual pathways of autophagy, mTOR, GLP-1, AMPK, Wnt, and WISP1.Expert review of clinical pharmacology · 2026Review
- Cellular Senescence in Neurodegeneration: From Cell Types to Therapeutic Opportunities.Biomedicines · 2026Review
- Agitation, Alzheimer's disease, and autophagy: mechanistic insights into aging pathways, gut microbiome, and artificial intelligence.Frontiers in immunology · 2026Review
- Running out the clock: Circadian rhythm dysfunction in cognitive disease.International review of neurobiology · 2026Review
- Neurosenescence, inflammaging and neuroinflammation in neurodegenerative disorders.Frontiers in aging · 2026Review
- Senotherapeutics for Brain Aging Management.Neurology international · 2025Review
- Dementia, mood disorders, and aging: Bridging new avenues of care through shared biological pathways.Aging advancesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Aging is a normal process causing deterioration in normal brain function and is inevitable. The aging process is described by the buildup of senescent cells and a decline in the ability to maintain essential homeostatic functions. Cellular aging represents a critical process where cells undergo cell cycle arrest in response to stress and neuronal damage. Many neurodegenerative disorders are closely linked to cellular senescence caused by oxidative stress, ROS generation, and DNA damage. Therefore, targeting cellular senescence is essential for the therapy of neurodegenerative disorders. Methods: This review outlines the understanding of cellular senescence, its role in the aging process, signaling pathways, autophagy, lysosomal biogenesis, and its contribution to various neurodegenerative disorders. Results: The findings highlight the relationship between cellular senescence and neurodegenerative disorders, emphasizing its pathological role. Current evidence indicates that senolytic drugs, notably phytochemicals such as dasatinib, quercetin, and fisetin, could serve as therapeutic approaches to target senescent cells and improve outcomes in neurodegenerative illnesses. Discussion: This review conclusively addresses the possibility of senolytic interventions for the treatment of neurodegenerative diseases. It will encourage researchers to identify novel compounds or phytochemicals that could be used as senolytic drugs for treating numerous neurodegenerative disorders.
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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.