Senolytic therapy alleviates Aβ-associated oligodendrocyte progenitor cell senescence and cognitive deficits in an Alzheimer’s disease model
Open accessAbstract
Neuritic plaques, a pathological hallmark in Alzheimer's disease (AD) brains, comprise extracellular aggregates of amyloid-beta (Aβ) peptide and degenerating neurites that accumulate autolysosomes. We found that, in the brains of patients with AD and in AD mouse models, Aβ plaque-associated Olig2- and NG2-expressing oligodendrocyte progenitor cells (OPCs), but not astrocytes, microglia, or oligodendrocytes, exhibit a senescence-like phenotype characterized by the upregulation of p21/CDKN1A, p16/INK4/CDKN2A proteins, and senescence-associated β-galactosidase activity. Molecular interrogation of the Aβ plaque environment revealed elevated levels of transcripts encoding proteins involved in OPC function, replicative senescence, and inflammation. Direct exposure of cultured OPCs to aggregating Aβ triggered cell senescence. Senolytic treatment of AD mice selectively removed senescent cells from the plaque environment, reduced neuroinflammation, lessened Aβ load, and ameliorated cognitive deficits. Our findings suggest a role for Aβ-induced OPC cell senescence in neuroinflammation and cognitive deficits in AD, and a potential therapeutic benefit of senolytic treatments.
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In preclinical studies, co-administration of Dasatinib and Quercetin improved aspects of physical function and cognition.
“In preclinical studies, co-administration of Dasatinib and Quercetin (DQ) improved aspects related to physical function (e.g., endurance and speed) and cognition (e.g., reduced neurofibrillary tangle density/neuron loss).7,15,24”
From A pilot study of senolytics to improve cognition and mobility in older adults at risk for Alzheimer's disease (2025) · cites this paper as [15]
The Results (page not provided) report that dasatinib plus quercetin improved Y-maze and water-maze performance in APP/PS1 Alzheimer’s-model mice, supporting the cognition portion. The paper does not report improved endurance or speed, or reduced neurofibrillary tangle density or neuron loss; its reported pathology improvement concerns Aβ plaques. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn mice, removing senescent cells genetically or pharmacologically improves function in models of neurodegenerative diseases such as Parkinson's and Alzheimer's.
“Importantly, clearance of Sncs either genetically or pharmacologically in mice leads to functional improvements in models of neurodegenerative diseases such as PD and AD (57–59).”
From Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span (2021) · cites this paper as [59]
The Results and Discussion (page not available in our copy) report that pharmacological senolytic treatment removed senescent cells and improved learning and memory in APP/PS1 Alzheimer’s-model mice. The Discussion also describes genetic clearance in other AD studies, but this paper does not report functional improvement after senescent-cell clearance in a Parkinson’s model, so it supports only part of the sentence attributed to the citation group. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSenescence has been observed in neurons, astrocytes, microglia, oligodendrocytes, and oligodendrocyte progenitor cells.
“Senescence has been observed in neurons, astrocytes, microglia, oligodendrocytes, and oligodendrocyte progenitor cells (57–59).”
From Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span (2021) · cites this paper as [59]
The Results (page unavailable) document senescent oligodendrocyte progenitor cells, and the Discussion (page unavailable) reports evidence of astrocyte and microglial senescence in other studies of tau-mutant mice. The paper does not establish senescence in mature oligodendrocytes or neurons; it cautions that neuronal SA-βGal staining can occur without other senescence phenotypes. (LLM, conf=0.87)
Experimental — accuracy not yet measuredThe INK-ATTAC and p16-3MR mouse models have substantially advanced knowledge about whether senescent cells contribute to ageing and age-related diseases in model organisms, covering conditions such as Parkinson disease, Alzheimer disease, atherosclerosis, idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, and osteoarthritis.
“These two mouse models have greatly accelerated our understanding of whether senescent cells contribute to ageing and age-related diseases, at least in model organisms, for numerous diseases, including Parkinson disease196, Alzheimer disease197,198, atherosclerosis175, idiopathic pulmonary fibrosis199, chronic obstructive pulmonary disease200 and osteoarthritis201.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [198]
The Discussion reports that removing senescent cells with senolytic treatment improved learning and memory in APP/PS1 Alzheimer’s disease mice, supporting the Alzheimer’s disease portion of the cited sentence. But the Methods describe a p16-ZsGreen reporter rather than INK-ATTAC or p16-3MR, and the Discussion proposes testing selective genetic elimination in Alzheimer’s disease mice as future work. This source therefore does not show that those two mouse models produced the Alzheimer’s disease finding attributed to it. (LLM, conf=0.89)
Experimental — accuracy not yet measuredPrevious studies have highlighted senescence in multiple brain cell types in AD.
“Previous studies have highlighted senescence in multiple brain cell types in AD [3, 16, 32, 52, 80].”
From Characterisation of premature cell senescence in Alzheimer's disease using single nuclear transcriptomics (2024) · cites this paper as [80]
The Abstract reports senescence-like changes in oligodendrocyte progenitor cells (OPCs) in patients with AD and AD mouse models. It explicitly says plaque-associated astrocytes, microglia, and oligodendrocytes did not show that phenotype; the Discussion places reports of astrocyte and microglial senescence in frontotemporal dementia models, not AD. Thus this source supports senescence in one brain cell type in AD, not multiple types. (LLM, conf=0.88)
Experimental — accuracy not yet measured
D + Q improves healthy lifespan in various laboratory model systems, including ADRD transgenic mice.
“This therapeutic approach, referred to as senolytic, improves healthy lifespan in various laboratory model systems, including ADRD transgenic mice [2,4,7].”
From Evaluation of exploratory fluid biomarkers from a phase 1 senolytic trial in mild Alzheimer's disease (2025) · cites this paper as [4]
The Results and Discussion report that D + Q improved learning and memory and reduced Aβ pathology in APP/PS1 Alzheimer’s-model mice. The study did not measure healthy lifespan in those mice or test D + Q across various laboratory model systems, so the broader claim is not established by this paper. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe introduction argues that senescent cells and their SASP products contribute to deficits in cognition and mobility.
“Recent evidence suggests that the accumulation of senescent cells, which can release a variety of pro-inflammatory, apoptotic, and toxic by-products, called the senescence-associated secretory phenotype (SASP), is one of the drivers of deficits in both cognition11, 12, 13, 14, 15, 16 and mobility.7,17, 18, 19, 20, 21, 22”
From A pilot study of senolytics to improve cognition and mobility in older adults at risk for Alzheimer's disease (2025) · cites this paper as [15]
Experimental — accuracy not yet measuredTreatment of an Alzheimer's disease mouse model with a senolytic agent improves memory and learning.
“treatment of an Alzheimer’s disease mouse model with a senolytic agent improved memory and learning ability160”
From Telomere dysfunction in ageing and age-related diseases (2022) · cites this paper as [160]
The authors conducted the first clinical trial of senolytic therapy for Alzheimer's disease.
“Given the compelling evidence provided by preclinical research6,19, coupled with the encouraging safety profiles reported in human studies of D + Q for other disease indications27,28, we conducted the first clinical trial of senolytic therapy for AD.”
From Senolytic therapy in mild Alzheimer's disease: a phase 1 feasibility trial (2023) · cites this paper as [19]
Other teams confirmed the association between tau and senescence in PS19 mice and effective senescent cell clearance by dasatinib plus quercetin in the Tg(APP/PS1) mouse model.
“Other research teams confirmed the association between tau and senescence in PS19 tau transgenic mice8 and the effective clearance of senescent cells using D + Q in the Tg(APP/PS1) Aβ-producing mouse model19.”
From Senolytic therapy in mild Alzheimer's disease: a phase 1 feasibility trial (2023) · cites this paper as [19]
OPC had been implicated in an earlier preclinical study.
“While we identified Olig2+ cells expressing some senescence markers, joint use of transcriptomic data was able to more probably ascribe this senescence signature predominantly to oligodendrocytes rather than OPC, which had been implicated in an earlier preclinical study [80].”
From Characterisation of premature cell senescence in Alzheimer's disease using single nuclear transcriptomics (2024) · cites this paper as [80]
Preclinical studies using different models have suggested that senolytic treatments can reduce the abundance of senescent cells, disease-relevant pathology and cognitive deficits.
“Preclinical studies using different models have suggested that senolytic treatments can reduce the abundance of senescent cells, disease-relevant pathology and cognitive deficits [8, 56, 80].”
From Characterisation of premature cell senescence in Alzheimer's disease using single nuclear transcriptomics (2024) · cites this paper as [80]
D + Q has demonstrated successful reduction in senescent cell burden, inflammatory SASP, AD-related neuropathological burden of tau-containing neurofibrillary tangles and Aβ plaques, and age-associated cognitive deficits in laboratory models.
“D + Q has demonstrated successful reduction in senescent cell burden, inflammatory SASP, AD-related neuropathological burden of tau-containing neurofibrillary tangles (NFTs) [2] and Aβ plaques [4], and age-associated cognitive deficits [8,9].”
From Evaluation of exploratory fluid biomarkers from a phase 1 senolytic trial in mild Alzheimer's disease (2025) · cites this paper as [4]
Senescent cell accumulation contributes to the progression of age-related disorders including Alzheimer's disease.
“Senescent cell accumulation contributes to the progression of age-related disorders including Alzheimer’s disease (AD).”
From Evaluation of exploratory fluid biomarkers from a phase 1 senolytic trial in mild Alzheimer's disease (2025) · cites this paper as [4]
An independent preclinical trial reported downregulation of IL1β in the brain in response to D+Q.
“An independent preclinical trial also reported downregulation of IL1β in the brain in response to D + Q [4].”
From Evaluation of exploratory fluid biomarkers from a phase 1 senolytic trial in mild Alzheimer's disease (2025) · cites this paper as [4]
SASP is a damaging byproduct of senescent cells, and a potential driver of Alzheimer's pathogenesis.
“A key contributor to the development and progression of inflammaging is the senescence associated secretory phenotype (SASP) – a damaging byproduct of senescent cells [63], and a potential driver of Alzheimer’s pathogenesis [64].”
The oligodendrocyte signatures observed here differ from those previously linked to multiple sclerosis and senescence.
“These oligodendrocyte signatures are distinct from those recently associated with multiple sclerosis21 and senescence43.”
From Human and mouse single-nucleus transcriptomics reveal TREM2-dependent and TREM2-independent cellular responses in Alzheimer’s disease (2020) · cites this paper as [43]
The delivery of senolytics in Alzheimer's disease mice reduces the amyloid-β load and the levels of proinflammatory factors, thereby enhancing cognitive function.
“The delivery of senolytics in AD mice reduces the Aβ load and the levels of proinflammatory factors, thereby enhancing cognitive funciton.430”
From Antiageing strategy for neurodegenerative diseases: from mechanisms to clinical advances (2025) · cites this paper as [430]
Emerging evidence suggests that senescent cells, including p16INK4A-positive senescent astrocytes and microglia and Aβ plaque-associated p16INK4A-positive oligodendrocyte progenitor cells, have a detrimental impact on neuronal loss and cognitive impairment in Alzheimer's disease mouse models.
“Emerging evidence suggests a detrimental impact of senescent cells, including p16INK4A-positive senescent astrocytes and microglia, and Aβ plaque-associated Olig2- and NG2-expressing p16INK4A-positive oligodendrocyte progenitor cells (OPCs) in neuronal loss and cognitive impairment in mouse models of AD (Bussian et al., 2018; Zhang et al., 2019).”
From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Zhang et al., 2019
Senolytic elimination of Aβ-associated senescent oligodendrocyte progenitor cells or Tau pathology-associated senescent glial cells ameliorates cognitive impairment in different Alzheimer's disease mouse models.
“Senolytic elimination of Aβ-associated senescent OPCs or Tau pathology-associated senescent glial cells ameliorates cognitive impairment in different AD mouse models (Bussian et al., 2018; Zhang et al., 2019).”
From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Zhang et al., 2019
Senolytic therapy provides beneficial effects in accelerated aging, tauopathy, and AD mouse models by reducing brain inflammation.
“The involvement of senescence and SASP in MCI and AD is further strengthened by experimental evidence that senolytic therapy provides beneficial effects in accelerated aging, 106 tauopathy, 22 and AD mouse models 25 by reducing brain inflammation.”
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 [25]
Senolytic therapy has shown promising results in various animal models, including tauopathies.
“Senolytic therapy has shown promising results in various animal models, including tauopathies.”
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 [25]
Eliminating senescent cells with senolytics reduces tau aggregation and inflammation and improves cognitive performance in vivo.
“eliminating senescent cells with senolytics reduces tau aggregation and inflammation and improves cognitive performance in vivo.”
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 [25]
Tau aggregates can trigger cellular senescence and inflammation.
“Several studies demonstrated that tau aggregates can trigger cellular senescence and inflammation”
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 [25]
The burden of senescent cells in the brain increases with advanced age and neurodegenerative diseases and occurs across neurons, microglia, astrocytes, oligodendrocyte precursor cells, and endothelial cells.
“The burden of senescent cells in the brain increases with advanced chronological age and neurodegenerative diseases, and occurs across cell types including neurons, microglia, astrocytes, oligodendrocyte precursor cells, and endothelial cells (28–32).”
From Senolytic Therapy to Modulate the Progression of Alzheimer's Disease (SToMP-AD): A Pilot Clinical Trial (2022) · cites this paper as [30]
An independent study validated that dasatinib plus quercetin clear senescent cells in the brain of a β-amyloid Alzheimer's disease mouse model.
“An independent study conducted by Zhang et al. validated the finding of D+Q clearance of senescent cells in the brain of an β-amyloid model of AD pathology (30).”
From Senolytic Therapy to Modulate the Progression of Alzheimer's Disease (SToMP-AD): A Pilot Clinical Trial (2022) · cites this paper as [30]
Across six transgenic Alzheimer's disease mouse models, orally administered senolytic drugs ablate brain senescent cells and alleviate Alzheimer's-relevant pathogenesis.
“To date, research conducted across six transgenic AD mouse models has demonstrated that orally administered senolytic drugs ablate senescent cells in the brain and alleviate AD-relevant pathogenesis (28–30, 32).”
From Senolytic Therapy to Modulate the Progression of Alzheimer's Disease (SToMP-AD): A Pilot Clinical Trial (2022) · cites this paper as [30]
The combination of dasatinib and quercetin eliminates senescent cells, reduces tau pathology, amyloid load, and neuroinflammation, and ameliorates cognitive impairment in preclinical studies.
“This drug combination eliminates the senescent cells (also known as “senolytic therapy”), reduces tau pathology, amyloid load, and neuroinflammation, and ameliorates cognitive impairment in preclinical studies [256, 257].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [256]
Senescent astrocytes and microglia accumulate in a tau-dependent mouse model of AD and contribute to cognitive decline.
“Senescent astrocytes and microglia accumulate in a tau‐dependent mouse model of AD where they contribute to cognitive decline in these mice (Bussian et al, 2018; Zhang et al, 2019).”
From The struggle of a good friend getting old: cellular senescence in viral responses and therapy (2021) · cites this paper as Zhang et al, 2019
CD38 is emerging as a key enzyme involved in inflammageing and senescence, which are strongly associated with neurodegenerative diseases.
“CD38 is emerging as a key enzyme involved in inflammageing and senescence45,105,106, which are strongly associated with neurodegenerative diseases124,128,168,169.”
From NAD+ metabolism and its roles in cellular processes during ageing (2021) · cites this paper as [169]
In APP/PS1 mutant transgenic mouse models, the quercetin-dasatinib combination acts by selective removal of senescent cells from the Aβ plaque environment, leading to reduced proinflammatory cytokine secretion and decreased Aβ concentration, with overall amelioration of cognitive disturbances.
“Successful repurposing in AD is supported by in vivo studies in amyloid precursor protein (APP)/PS1 mutant transgenic mouse models.The combination seems to act by the selective removal of senescent cells from the Aβ plaque environment, leading to a reduction of proinflammatory cytokine secretion and a decrease of Aβ concentration, with an overall amelioration of cognitive disturbances.66”
From From combinations to multitarget-directed ligands: A continuum in Alzheimer’s disease polypharmacology (2021) · cites this paper as [66]
Pharmacological and genetic elimination of senescent cells has shown therapeutic benefits for Alzheimer's disease pathology in mouse models of tau and amyloid pathology.
“the pharmacological and genetic elimination of senescent cells has shown therapeutic benefits for AD pathology in mouse models of tau and amyloid pathology [11, 83, 122].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [122]
Senotherapy ameliorated phenotypes in all of these mouse models, attenuating tau phosphorylation and aggregation, reducing neuroinflammation and amyloid β plaque load, and improving cognitive deficits.
“Senotherapy has been shown to ameliorate phenotypes in all of these mouse models, attenuating tau phosphorylation and aggregation, 39 reducing neuroinflammation and amyloid β plague load, and improving cognitive deficits.40”
From The costs and benefits of senotherapeutics for human health (2022) · cites this paper as [40]
Senescent OLIG2- and NG2-expressing oligodendrocyte progenitor cells contribute to cognitive impairment in an Alzheimer's disease mouse model.
“Zhang et al. employed a senolytic cocktail of dasatinib plus quercetin (D + Q) to validate that senescent OLIG2- and NG2-expressing oligodendrocyte progenitor cells (OPCs) contribute to cognitive impairment in an AD mouse model [56].”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [56]
Senescent-like brain cells are identified in murine models of AD and tauopathy, and their removal via senolytic drugs mitigates pathology and improves cognition.
“More recently, researchers have identified senescent‐like brain cells in murine models of AD and tauopathy, and their removal via senolytic drugs seems to mitigate pathology and improve cognition (Bussian et al, 2018; Musi et al, 2018; Zhang et al, 2019; Ogrodnik et al, 2021).”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Zhang et al, 2019
Senescent-like phenotypes are identified in oligodendrocyte precursor cells in APP/PS1 mice, and their removal mitigates amyloid load and cognitive decline.
“Senescent‐like phenotypes have also been identified in oligodendrocyte precursor cells (OPCs) in APP/PS1 mice, and their removal has been shown to mitigate amyloid load and cognitive decline (Zhang et al, 2019).”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Zhang et al, 2019
Removal of senescent cells in the brain mitigates NFT burden, amyloid burden, neuronal loss, and cognitive decline in mouse models of tauopathy, AD, PD, and normal aging.
“It has since been shown that removal of senescent cells in the brain mitigates neurofibrillary tangle (NFT) burden, amyloid burden, neuronal loss, and cognitive decline in mouse models of tauopathy (Bussian et al, 2018; Musi et al, 2018), AD (Zhang et al, 2019), PD (Chinta et al, 2018), and normal aging (Ogrodnik et al, 2021).”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Zhang et al, 2019
Putative senescent states have been suggested in microglia, neurons, astrocytes, and oligodendrocyte progenitor cells with aging and in various disease contexts.
“Putative senescent states have been suggested in a variety of neural subpopulations with aging and in various disease contexts, including microglia [26–30], neurons [31–33], astrocytes [26,34,35], and oligodendrocyte progenitor cells [36].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [36]
Each of these studies demonstrated pathology mitigation following pharmacological removal of senescent cells.
“Regardless of the hypothesized identity of the senescent population, each of these studies demonstrated pathology mitigation following pharmacological removal of senescent cells [26,33,36].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [36]
Recent studies have produced evidence for senescence in neurons and oligodendrocyte progenitors in mouse models of tauopathy and AD.
“Recent studies have produced evidence for senescence in neurons and oligodendrocyte progenitors in other mouse models of tauopathy and AD [33,36].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [36]
Some senolytics have been effectively used in mouse models of neurological disease to alleviate pathology, including dasatinib and quercetin and navitoclax, which has led to senolytic therapies entering clinical trials for modulation of AD.
“Nevertheless, some senolytics have been effectively used in mouse models of neurological disease to alleviate pathology including dasatinib and quercetin [36] and navitoclax [26], which has led to senolytic therapies entering clinical trials for the modulation of AD [171].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [36]
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- Authors
- Zhang, P., Kishimoto, Y., Grammatikakis, I., Gottimukkala, K., Cutler, R. G., Zhang, S., Abdelmohsen, K., Bohr, V. A., Misra Sen, J., Gorospe, M., & Mattson, M. P.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Zhang, Peisu
- Mattson, Mark P.
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2019-04-01
- Volume
- 22
- Issue
- 5
- Pages
- 719-728
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC6605052
- OpenAlex
- W2928157366
- Cited by
- 977
- References
- 48
- Citations by year
- 2026: 109 · 2025: 157 · 2024: 168 · 2023: 135 · 2022: 133 · 2021: 131 · 2020: 118 · 2019: 26
- FWCI
- 69.44
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (Z99 AG999999)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- senolytic therapy, Alzheimer's disease, amyloid-beta, oligodendrocyte precursor cells, cellular senescence, neuroinflammation, cognitive impairment, senescent cell clearance, Olig2, NG2, replicative senescence, senescence-associated β-galactosidase, CDKN1A/p21, CDKN2A/p16, amyloid plaques
- MeSH terms
- Dasatinib, Oligodendrocyte Precursor Cells, Alzheimer Disease, Animals, Disease Models, Animal, Female, Male, Mice, Transgenic, Quercetin, Amyloid beta-Peptides, Prosencephalon, Cellular Senescence, Maze Learning, Plaque, Amyloid
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