Cellular senescence at the crossroads of inflammation and Alzheimer's disease
Open accessAbstract
Aging is a key risk factor for Alzheimer's disease (AD), but the reasons for this association are not well understood. Senescent cells accumulate in aged tissues and have been shown to play causal roles in age-related pathologies through their proinflammatory secretome. The question arises whether senescence-induced inflammation might contribute to AD and bridge the gap between aging and AD. Here, we highlight the role of cellular senescence as a driver of the aging phenotype, and discuss the current evidence that connects senescence with AD and neurodegeneration.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Accumulation of senescent cells in aging tissues can be accelerated by chronic inflammation.
“Accumulation of senescent cells in aging tissues can be accelerated by a wide range of cell stressors, including chronic inflammation [27].”
From Characterisation of premature cell senescence in Alzheimer's disease using single nuclear transcriptomics (2024) · cites this paper as [27]
The Concluding remarks say that neuroinflammation can induce senescence in neurons and glial cells in Alzheimer’s disease, supporting an inflammation-to-senescence link in that setting. But the section “Cellular senescence as a source of chronic inflammation” describes senescent-cell accumulation as reinforcing inflammation; it does not establish that chronic inflammation accelerates accumulation across aging tissues. Page numbers are unavailable in our copy. (LLM, conf=0.78)
Experimental — accuracy not yet measuredCellular senescence plays a crucial role in Alzheimer's disease pathogenesis.
“Cellular senescence [25] plays a crucial role in AD pathogenesis.”
From Oral Microbially-Induced Small Extracellular Vesicles Cross the Blood–Brain Barrier (2024) · cites this paper as [25]
The ‘Pathology-induced senescence exacerbates AD’ section says senescent cells may accelerate AD progression through a positive feedback loop. But ‘Potential role of cellular senescence in AD’ describes the evidence as emerging and its proposed role as a hypothesis. Calling senescence a crucial factor in AD pathogenesis states that role more definitively than the review does. (LLM, conf=0.84)
Experimental — accuracy not yet measuredSASP composition and dynamics may contribute to disease heterogeneity and the rate of cognitive decline.
“indicating that SASP composition and dynamics may contribute to disease heterogeneity and the rate of cognitive decline. 70”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [70]
Senescent cells produce a distinct inflammatory secretome.
“Senescent cells produce a distinct inflammatory secretome and have been found to accumulate with age and in many diseases; potentially contributing to pathology [17–21].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [21]
Senescent cells accumulate with age and in many diseases, potentially contributing to pathology.
“Senescent cells produce a distinct inflammatory secretome and have been found to accumulate with age and in many diseases; potentially contributing to pathology [17–21].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [21]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 155 · Cited by 236
Research works printed but not linked: 2
- Preman, P., et al. (2020) Human iPSC-derived astrocytes transplanted into the mouse brain display three morphological responses to amyloid-β plaques. bioRxiv, 2020.2011.2019.389023
- Olona, A., et al. (2020) Cardiac glycosides cause selective cytotoxicity in human macrophages and ameliorate white adipose tissue homeostasis. bioRxiv 105
- Authors
- Guerrero, A., De Strooper, B., & Arancibia-Cárcamo, I. L.
- Affiliations
- The Francis Crick Institute (GB)
- Venue
- Trends in Neurosciences
- Publisher
- Elsevier BV
- Published
- 2021-09
- Volume
- 44
- Issue
- 9
- Pages
- 714-727
- ISSN
- 0166-2236 (ISSN-L)
- OpenAlex
- W3187230189
- Cited by
- 236
- References
- 155
- Citations by year
- 2026: 29 · 2025: 45 · 2024: 62 · 2023: 54 · 2022: 38 · 2021: 7
- FWCI
- 5.37
- Type
- journal article
- Language
- en
- Open access
- green
- lirias.kuleuven.be
- Licence
- Locations
- Trends in Neurosciences (publishedVersion)
- PubMed (publishedVersion)
- Lirias (KU Leuven) (submittedVersion, other-oa)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Alzheimer's Society
- Alzheimer’s Research UK
- Desert Research Institute
- Medical Research Council
- UK Dementia Research Institute
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- cellular senescence, Alzheimer's disease, inflammation, aging, senescence-associated secretome, neurodegeneration, age-related diseases
- MeSH terms
- Aged, Aging, Alzheimer Disease, Humans, Inflammation, Phenotype, Cellular Senescence
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
