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Cited by 267Alzheimer's disease research and treatmentsTelomeres, Telomerase, and SenescenceDementia and Cognitive Impairment Research

Aging, Cellular Senescence, and Alzheimer’s Disease

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Liu, Rui-Ming·2022·International Journal of Molecular Sciences
DOI 10.3390/ijms23041989PMC PMC8874507
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Abstract

Aging is the greatest risk factor for late-onset Alzheimer’s disease (LOAD), which accounts for >95% of Alzheimer’s disease (AD) cases. The mechanism underlying the aging-related susceptibility to LOAD is unknown. Cellular senescence, a state of permanent cell growth arrest, is believed to contribute importantly to aging and aging-related diseases, including AD. Senescent astrocytes, microglia, endothelial cells, and neurons have been detected in the brain of AD patients and AD animal models. Removing senescent cells genetically or pharmacologically ameliorates β-amyloid (Aβ) peptide and tau-protein-induced neuropathologies, and improves memory in AD model mice, suggesting a pivotal role of cellular senescence in AD pathophysiology. Nonetheless, although accumulated evidence supports the role of cellular senescence in aging and AD, the mechanisms that promote cell senescence and how senescent cells contribute to AD neuropathophysiology remain largely unknown. This review summarizes recent advances in this field. We believe that the removal of senescent cells represents a promising approach toward the effective treatment of aging-related diseases, such as AD.

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  • A growing body of evidence in human and animal studies supports a role of cellular senescence in neurodegeneration and memory loss in Alzheimer's disease.

    “A growing body of evidence in human and animal studies supports a role of cellular senescence in neurodegeneration and memory loss in AD [16].”

    From Oral Microbially-Induced Small Extracellular Vesicles Cross the Blood–Brain Barrier (2024) · cites this paper as [16]

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Authors
Liu, R.-M.
Affiliations
University of Alabama at Birmingham (US)
Corresponding author
Liu, Rui-Ming
ORCID
Liu, Rui-Ming
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2022-02-11
Volume
23
Issue
4
Pages
1989
ISSN
1422-0067 (ISSN-L)
DOI
10.3390/ijms23041989
PMC
PMC8874507
OpenAlex
W4213324992
Cited by
267
References
39
Citations by year
2026: 39 · 2025: 84 · 2024: 78 · 2023: 50 · 2022: 16
FWCI
7.81
Type
journal article
Language
en
Open access
Licence
Locations
  • International Journal of Molecular Sciences (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • U.S. Department of Defense
  • National Institute on Aging (R01AG077395)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
cellular senescence, Alzheimer's disease, aging, senolytics, senescent cells, senescence-associated secretory phenotype, astrocytes, microglia, amyloid-beta, tau protein, memory impairment, late-onset Alzheimer's disease
MeSH terms
Aging, Alzheimer Disease, Animals, Astrocytes, Brain, Humans, Neurons, 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 ›

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