The DOI matches its Crossref record; 191 of the 191 references it cites were found in a registry or an index.
Are there roles for brain cell senescence in aging and neurodegenerative disorders?
Open accessAbstract
The term cellular senescence was introduced more than five decades ago to describe the state of growth arrest observed in aging cells. Since this initial discovery, the phenotypes associated with cellular senescence have expanded beyond growth arrest to include alterations in cellular metabolism, secreted cytokines, epigenetic regulation and protein expression. Recently, senescence has been shown to play an important role in vivo not only in relation to aging, but also during embryonic development. Thus, cellular senescence serves different purposes and comprises a wide range of distinct phenotypes across multiple cell types. Whether all cell types, including post-mitotic neurons, are capable of entering into a senescent state remains unclear. In this review we examine recent data that suggest that cellular senescence plays a role in brain aging and, notably, may not be limited to glia but also neurons. We suggest that there is a high level of similarity between some of the pathological changes that occur in the brain in Alzheimer's and Parkinson's diseases and those phenotypes observed in cellular senescence, leading us to propose that neurons and glia can exhibit hallmarks of senescence previously documented in peripheral tissues.
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“Data have shown that various parts of the brain in patients with neurodegenerative diseases are characterised by increased expression of senescence markers.70”
From The costs and benefits of senotherapeutics for human health (2022) · cites this paper as [70]
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Mukvych, V. V., Lyashenko, V. P., & Lukashov, S. М. (2018) · Regulatory Mechanisms in Biosystems · doi:10.15421/021889 · Cited by 1
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Metadata
- Authors
- Tan, F. C. C., Hutchison, E. R., Eitan, E., & Mattson, M. P.
- Affiliations
- National Institute on Aging (US)
- Corresponding author
- Hutchison, Emmette R.
- Eitan, Erez
- Venue
- Biogerontology
- Published
- 2014-10-11
- Volume
- 15
- Issue
- 6
- Pages
- 643-660
- ISSN
- 1389-5729 (ISSN-L)
- 1573-6768
- PMC
- PMC4264619
- OpenAlex
- W1977085416
- Cited by
- 116
- References
- 191
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 4 · 2023: 8 · 2022: 14 · 2021: 12 · 2020: 15 · 2019: 16 · 2018: 19 · 2017: 10 · 2016: 4 · 2015: 2 · 2014: 2
- FWCI
- 0.70
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Biogerontology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (Z99 AG999999)
- 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, brain aging, neurodegenerative diseases, Alzheimer's disease, Parkinson's disease, neuronal senescence, senescence-associated secretory phenotype, epigenetic regulation, postmitotic neurons, embryonic development
- MeSH terms
- Aged, Aging, Animals, Brain, Humans, Neuroglia, Neurons, Cellular Senescence, Neurodegenerative Diseases, Epigenesis, Genetic, Mice
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