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Cellular senescence and Alzheimer disease: the egg and the chicken scenario
Saez-Atienzar S, Masliah E.. Nature reviews. Neuroscience, 2020-06-29
Topic: Amyloid, tau and blood-test diagnosis
Plain-language summary
Globally, 50 million people live with dementia, with Alzheimer disease (AD) being responsible for two-thirds of the total cases. As ageing is the main risk factor for dementia-related neurodegeneration, changes in the timing or nature of the cellular hallmarks of normal ageing might be key to understanding the events that convert normal ageing into neurodegeneration. Cellular senescence is a candidate mechanism that might be important for this conversion.
What this study adds
Evidence grade: Low
This is a narrative review. This review discusses cellular senescence as a possible mechanism converting normal ageing into neurodegeneration, including in neurons, astrocytes and microglia. It offers no treatment, cure or prevention.
Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Saez-Atienzar, S., & Masliah, E. (2020). Cellular senescence and Alzheimer disease: the egg and the chicken scenario. Nature reviews. Neuroscience. https://doi.org/10.1038/s41583-020-0325-z
Vancouver
Saez-Atienzar S, Masliah E. Cellular senescence and Alzheimer disease: the egg and the chicken scenario. Nature reviews. Neuroscience. 2020. doi:10.1038/s41583-020-0325-z. PMID: 32601397.
BibTeX
@article{saezatienzar2020-32601397,
author = {Saez-Atienzar, S. and Masliah, E.},
title = {{Cellular senescence and Alzheimer disease: the egg and the chicken scenario}},
journal = {Nature reviews. Neuroscience},
year = {2020},
doi = {10.1038/s41583-020-0325-z},
pmid = {32601397},
url = {https://doi.org/10.1038/s41583-020-0325-z}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- As ageing is the main risk factor for dementia-related neurodegeneration, changes in the timing or nature of the cellular hallmarks of normal ageing might be key to understanding the events that convert normal ageing into neurodegeneration.
- Cellular senescence is a candidate mechanism that might be important for this conversion.
- Under persistent stress, as occurs in ageing, both postmitotic cells - including neurons - and proliferative cells - such as astrocytes and microglia, among others - can engender a state of chronic cellular senescence that is characterized by the secretion of pro-inflammatory molecules that promote the functional decline of tissues and organs.
- Ablation of senescent cells has been postulated as a promising therapeutic venue to target the ageing phenotype and, thus, prevent or mitigate ageing-related diseases.
Why it matters
This review discusses cellular senescence as a possible mechanism converting normal ageing into neurodegeneration, including in neurons, astrocytes and microglia. It offers no treatment, cure or prevention.
Study details
- Evidence strengthLow
How this study scored 50/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Nature reviews. Neuroscience) |
| Journal's citation record | 4 / 4 | Nature reviews. Neuroscience: journal h-index 572 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2020 — within 10 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 255 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 31.9 citations a year over 8 year(s) since 2020 |
| Impact for its field and year | 3 / 6 | Cited 5.9× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 3 / 4 | Cited 116 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Eliezer Masliah: h-index 195 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | National Institutes of Health: institution h-index 2,723 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 32601397) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 50 / 100 | — |
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