Increased post-mitotic senescence in aged human neurons is a pathological feature of Alzheimer’s disease
Open accessAbstract
The concept of senescence as a phenomenon limited to proliferating cells has been challenged by growing evidence of senescence-like features in terminally differentiated cells, including neurons. The persistence of senescent cells late in life is associated with tissue dysfunction and increased risk of age-related disease. We found that Alzheimer's disease (AD) brains have significantly higher proportions of neurons that express senescence markers, and their distribution indicates bystander effects. AD patient-derived directly induced neurons (iNs) exhibit strong transcriptomic, epigenetic, and molecular biomarker signatures, indicating a specific human neuronal senescence-like state. AD iN single-cell transcriptomics revealed that senescent-like neurons face oncogenic challenges and metabolic dysfunction as well as display a pro-inflammatory signature. Integrative profiling of the inflammatory secretome of AD iNs and patient cerebral spinal fluid revealed a neuronal senescence-associated secretory phenotype that could trigger astrogliosis in human astrocytes. Finally, we show that targeting senescence-like neurons with senotherapeutics could be a strategy for preventing or treating AD.
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Features of premature senescence associated with DSBs and p16 expression have been described in post-mitotic cells such as neurons.
“However, features of premature senescence associated particularly with DNA double-strand breaks (DSBs) and p16 expression also have been described in post-mitotic cells such as neurons[16, 18, 29].”
From Characterisation of premature cell senescence in Alzheimer's disease using single nuclear transcriptomics (2024) · cites this paper as [29]
The Results section on the human prefrontal cortex reports p16-positive, senescent-like neurons in aged brains, with more in Alzheimer’s disease, and the oncogene experiments show that senescence can be induced in neurons. The paper does not establish that this neuronal senescence is associated with DNA double-strand breaks; its discussion of a DNA damage response after Ras treatment is speculative, and the double-strand-break passage found is a reference title. No page numbers were available in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredNo AD hallmark neuropathology was shown in neurons directly induced from individuals with AD through NGN2/ASCL1 overexpression.
“but no AD hallmark neuropathology was shown.”
From Modeling late-onset Alzheimer’s disease neuropathology via direct neuronal reprogramming (2024) · cites this paper as [24]
The Results section on senescent patterns in AD induced neurons (page unavailable) confirms that neurons from AD patients were generated by direct Ngn2/Ascl1 conversion. The Results section on in vitro senescence markers reports AD-associated neuronal senescence, but our copy does not establish whether hallmark neuropathology such as amyloid plaques or tau tangles was shown or absent in those neurons. (LLM, conf=0.78)
Experimental — accuracy not yet measuredThese severely affected donors had lower transcription and reduced chromatin accessibility that may correspond to senescent states or global epigenome dysregulation that is indicative of cell identity loss.
“These severely affected donors had lower transcription and reduced chromatin accessibility that may correspond to senescent states97, or global epigenome dysregulation that is indicative of cell identity loss98.”
From Integrated multimodal cell atlas of Alzheimer’s disease (2024) · cites this paper as [97]
The Results section on senescent transcriptomic and epigenomic patterns (page unavailable) links neuronal senescence to altered transcription and chromatin, supporting the suggested connection to senescent states. But it reports increased expression and chromatin accessibility at senescence genes in Alzheimer’s-derived neurons, not that lower transcription and reduced accessibility characterize the senescent state. The cell-identity-loss clause is attached to citation 98, not this source. (LLM, conf=0.84)
Experimental — accuracy not yet measuredRecent studies have directly induced neurons from individuals with AD through NGN2/ASCL1 overexpression.
“Recent studies have directly induced neurons from individuals with AD through NGN2/ASCL1 overexpression.”
From Modeling late-onset Alzheimer’s disease neuropathology via direct neuronal reprogramming (2024) · cites this paper as [24]
Neurons directly induced from individuals with AD through NGN2/ASCL1 overexpression exhibited age-associated dysregulations such as instability of mature neuronal fate, increased cellular senescence, and metabolic shifts.
“These neurons exhibited several age-associated dysregulations such as instability of mature neuronal fate, increased cellular senescence, and metabolic shifts (11, 24, 25)”
From Modeling late-onset Alzheimer’s disease neuropathology via direct neuronal reprogramming (2024) · cites this paper as [24]
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Kumar, M., Ray, S., & Sil, S. (2025) · Extracellular Vesicles and Circulating Nucleic Acids · doi:10.20517/evcna.2025.65 · Cited by 8 · see citing works
The Biological Intersection Between Chemotherapy-Related Cognitive Impairment and Alzheimer Disease
Torre, M., Zanella, C. A., & Feany, M. Β. (2025) · American Journal Of Pathology · doi:10.1016/j.ajpath.2024.12.013 · Cited by 7 · see citing works
Zhu, Q., Song, Y., Qian, Y., Zhang, R., Xue, J., & Hou, Y. (2025) · Ageing and Neurodegenerative Diseases · doi:10.20517/and.2025.25 · Cited by 6 · see citing works
Telomeric DNA damage response mediates neurotoxicity of Aβ42 oligomers in Alzheimer’s disease
Sepe, S., Rey, F., Mancheno-Ferris, A., Bigi, A., Fani, G., Damiani, D., Cabrini, M., Marinelli, E., Aguado, J., Contu, L., et al. (2025) · The EMBO Journal · doi:10.1038/s44318-025-00521-1 · Cited by 7 · see citing works
Cellular senescence as a therapeutic target for aging intervention
Bi, Y., & Ji, G. (2026) · Biomedical Journal · doi:10.1016/j.bj.2026.100948 · Cited by 7 · see citing works
Jiao, B., Zhang, H., Jiang, H., Liu, S., Wang, Y., Chen, Y., Duan, H., Niu, Y., Shen, M., Wang, H., et al. (2024) · Ecotoxicology and Environmental Safety · doi:10.1016/j.ecoenv.2024.116174 · Cited by 7 · see citing works
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Epigenome erosion in Alzheimer’s disease brain cells and induced neuronsPreprint
Wang, B.-A., Jones, J. R., Zhou, J., Tian, W., Wu, Y., Wang, W., Berube, P., Bartlett, A., Castanon, R., Nery, J. R., et al. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.10.15.562394 · Cited by 7 · see citing works
Self-citationWang, S., Li, B., Cai, Z., Hugo, C., Li, J., Sun, Y. E., Lü, Q., Remaley, A. T., Julia, T. C. W., Chui, H. C., et al. (2024) · Research Square · doi:10.21203/rs.3.rs-4373201/v1 · Cited by 7 · see citing works
- Authors
- Herdy, J. R., Traxler, L., Agarwal, R. K., Karbacher, L., Schlachetzki, J. C. M., Boehnke, L., Zangwill, D., Galasko, D., Glass, C. K., Mertens, J., & Gage, F. H.
- Affiliations
- Salk Institute for Biological Studies (US)
- Universität Innsbruck (AT)
- University of California San Diego (US)
- Corresponding author
- Herdy, Joseph R.
- Gage, Fred H.
- ORCID
- Venue
- Cell Stem Cell
- Publisher
- Elsevier BV
- Published
- 2022-12
- Volume
- 29
- Issue
- 12
- Pages
- 1637-1652.e6
- ISSN
- 1875-9777 (ISSN-L)
- 1934-5909
- PMC
- PMC10093780
- OpenAlex
- W4310496865
- Cited by
- 208
- References
- 79
- Citations by year
- 2026: 59 · 2025: 63 · 2024: 63 · 2023: 23
- FWCI
- 23.04
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 365 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell stem cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- Michael J. Fox Foundation for Parkinson's Research
- California Institute for Regenerative Medicine
- American Heart Association (H2020, 19PABH134610000, 19PABHI34610000)
- BrightFocus Foundation (A2019562S, ERC-STG-2019-852086, H2020-MSCA-IF-2017-797205)
- Waitt Foundation
- European Commission (H2020-MSCA-IF-2017., H2020, 797205, H2020‐MSCA‐IF, H2020-MSCA)
- Austrian Science Fund (FWF-I5057)
- National Institutes of Health (P30 014195, RT2-01927, 1s10od023689-01a1, H2020, AG062429, AG051449)
- University of California, San Diego
- Horizon 2020 Framework Programme (H2020-MSCA, H2020-MSCA-IF-2017)
- National Institute on Aging (K99AG056679, R01AG056306, R01AG057706, R01AG056511, T32AG000216, P30AG062429, RF1AG056306, P01AG051449, R37AG072502)
- National Cancer Institute (S10-OD023689, P30014195)
- National Institute of General Medical Sciences (T32GM007198)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- neuronal senescence, Alzheimer's disease, senescence-associated secretory phenotype, senotherapeutics, astrocyte activation, neuroinflammation, senescence markers
- MeSH terms
- Aged, Alzheimer Disease, Astrocytes, Brain, Humans, Neurons, Oncogenes
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.
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