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Clearance of senescent glial cells prevents tau-dependent pathology and cognitive decline
Open accessAbstract
Cellular senescence, which is characterized by an irreversible cell-cycle arrest 1 accompanied by a distinctive secretory phenotype 2, can be induced through various intracellular and extracellular factors. Senescent cells that express the cell cycle inhibitory protein p16 INK4A have been found to actively drive naturally occurring age-related tissue deterioration 3,4 and contribute to several diseases associated with ageing, including atherosclerosis 5 and osteoarthritis 6. Various markers of senescence have been observed in patients with neurodegenerative diseases 7-9; however, a role for senescent cells in the aetiology of these pathologies is unknown. Here we show a causal link between the accumulation of senescent cells and cognition-associated neuronal loss. We found that the MAPT P301S PS19 mouse model of tau-dependent neurodegenerative disease 10 accumulates p16 INK4A-positive senescent astrocytes and microglia. Clearance of these cells as they arise using INK-ATTAC transgenic mice prevents gliosis, hyperphosphorylation of both soluble and insoluble tau leading to neurofibrillary tangle deposition, and degeneration of cortical and hippocampal neurons, thus preserving cognitive function. Pharmacological intervention with a first-generation senolytic modulates tau aggregation. Collectively, these results show that senescent cells have a role in the initiation and progression of tau-mediated disease, and suggest that targeting senescent cells may provide a therapeutic avenue for the treatment of these pathologies.
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In the citing paper
“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 [58]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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 [58]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Genetic clearance of senescent cells or senolytic treatment in tauopathy mouse models mitigated cognitive decline and neurode-generation158,159”
From Telomere dysfunction in ageing and age-related diseases (2022) · cites this paper as [158]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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 [197]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Cellular senescence contributes to Alzheimer’s disease (AD) pathogenesis.”
From Senolytic therapy in mild Alzheimer's disease: a phase 1 feasibility trial (2023) · cites this paper as [8]
Experimental — accuracy not yet measured
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“However, studies in preclinical models of various CNS disorders have demonstrated reduced gliosis and neuroinflammation with senescent cell clearance, for example,6,8,17,19,25,50.”
From Senolytic therapy in mild Alzheimer's disease: a phase 1 feasibility trial (2023) · cites this paper as [8]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Furthermore, prior research conducted on postmortem brain tissue from individuals with AD has identified senescent astrocytes16, and mouse models have demonstrated that they are cleared with senolytic treatment8,17.”
From Senolytic therapy in mild Alzheimer's disease: a phase 1 feasibility trial (2023) · cites this paper as [8]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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 Bussian et al., 2018
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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 [22]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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 [22]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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 Bussian et al, 2018
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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 [8]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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 [11]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Bussian et al. reported that clearance of p16+ senescent astrocytes and microglia using INKATTAC transgene restrains gliosis, super-phosphorylation of both soluble and insoluble tau resulting in neurofibrillary tangle deposition and degeneration of cortical and hippocampal neurons, thus restoring cognitive function.”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [18]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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 Bussian et al, 2018
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Senescent cells accumulate with ageing and age-associated diseases, limiting lifespan and healthspan in mice11–16.”
From Senescence atlas reveals an aged-like inflamed niche that blunts muscle regeneration (2023) · cites this paper as [12]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In aged organisms, senescent cells can contribute to a variety of age- related pathologies, including pulmonary fibrosis, biliary liver damage, arteriosclerosis, retinopathy, osteoarthritis, dementia and diabetes mellitus 13-19 .”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [17]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“These cells are implicated in sterile inflammation, wound healing, and age-related processes, including neurodegeneration”
From Cross-Species Single-Cell Analysis Reveals Divergence of the Primate Microglia Program (2019) · cites this paper as Bussian et al., 2018
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Numerous human and rodent model studies have highlighted the important role of astrocytes in AD and tau pathology, with astrocyte activation occurring prior to large scale NFT formation, synaptic dysfunction, and neuronal loss (Bussian et al., 2018; Shi et al., 2017; Yoshiyama et al., 2007).”
From Selective removal of astrocytic APOE4 strongly protects against tau-mediated neurodegeneration and decreases synaptic phagocytosis by microglia (2021) · cites this paper as Bussian et al., 2018
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“which suggests that cellular senescence has a causative effect in this pathology”
From Telomere dysfunction in ageing and age-related diseases (2022) · cites this paper as [158]
The cited source says what the claim attributes to it.
In the citing paper
“In the context of aging and neurodegenerative disease, senescent cell accumulation has been identified in multiple cell types within the central nervous system (CNS), including neurons6,7,14,15, astrocytes16,17, microglia8,18, oligodendrocyte precursor cells19 and endothelial cells20.”
From Senolytic therapy in mild Alzheimer's disease: a phase 1 feasibility trial (2023) · cites this paper as [8]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“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 [8]
The cited source says what the claim attributes to it.
In the citing paper
“Increased numbers of p16-positive astrocytes and microglia also have been reported with tau-mediated disease initiation and progression in a mouse model [8].”
From Characterisation of premature cell senescence in Alzheimer's disease using single nuclear transcriptomics (2024) · cites this paper as [8]
The cited source says what the claim attributes to it.
In the citing paper
“Excessive senescent cells have been demonstrated to play a causal role in driving ageing [26] and chronic diseases [18] using genetic and pharmacologic approaches.”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [18]
The cited source says what the claim attributes to it.
In the citing paper
“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 [26]
The cited source says what the claim attributes to it.
In the citing paper
“Removal of the p16Ink4a-positive senescent cells, for instance, using a suicide gene under the regulation of the Cdkn2a promoter has been shown to attenuate progression of age-related decline and preserve cognitive function in both an accelerated aging AD mouse model and a tauopathy mouse model (Baker et al., 2011; Bussian et al., 2018).”
From Inhibiting USP16 rescues stem cell aging and memory in an Alzheimer’s model (2022) · cites this paper as Bussian et al., 2018
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“fibroblasts present not only papillary and reticular phenotypes, but also heterogeneous populations if studied at the single-cell level58,59.”
From Guidelines for minimal information on cellular senescence experimentation in vivo (2024) · cites this paper as [59]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Keratinocytes display different properties across different strata of the epidermis”
From Guidelines for minimal information on cellular senescence experimentation in vivo (2024) · cites this paper as [59]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Keratinocytes and fibroblasts can be further divided into different subtypes.”
From Guidelines for minimal information on cellular senescence experimentation in vivo (2024) · cites this paper as [59]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“retrotransposon expression has in fact been shown to have a role in DNA damage (Yousefzadeh et al. 2021), cellular senescence (Bussian et al. 2018, De Cecco et al. 2019b, Li et al. 2013, Musi et al. 2018), and inflammatory signaling (Franceschi et al. 2018, Gulen et al. 2023), which are well-described features of both aging and some neurodegenerative disorders”
From The Role of Retrotransposons and Endogenous Retroviruses in Age-Dependent Neurodegenerative Disorders (2024) · cites this paper as Bussian et al. 2018
Experimental — accuracy not yet measuredIn the citing paper
“The aggregation of misfolded proteins, including Aβ plaques and tau neurofibrillary tangles, may also promote neuronal and glial senescent phenotypes (171), as do other common facets of neurodegeneration, such as mitochondrial dysfunction and abnormal proteostasis (22, 172, 173).”
From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [22]
In the citing paper
“These persisting senescent cells have been recently tied to multiple chronic diseases other than atherosclerosis, including diabetes mellitus,85 obesity,85 Alzheimer’s disease,86 heart failure,10,87 idiopathic pulmonary fibrosis,88,89 chronic obstructive pulmonary disease,90 chronic kidney disease,91 cancer,92 and osteoarthritis.93”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [86]
In the citing paper
“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 Bussian et al., 2018
In the citing paper
“Recent studies in humans and animal models demonstrate that aging is associated with increased accumulation of senescent cells.”
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 [22]
In the citing paper
“Various endogenous and exogenous stressors (eg, pathological tau aggregates) can induce senescence in different types of brain cells. 22 , 23 , 24 , 25”
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 [22]
In the citing paper
“selective clearance of senescent cells extends the healthy lifespan in aged animals and also prevents AD‐associated brain pathology and cognitive decline, 22 , 23 , 24 , 25”
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 [22]
In the citing paper
“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 [22]
In the citing paper
“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 [22]
In the citing paper
“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 [128]
In the citing paper
“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 [39]
In the citing paper
“work establishing a role for senescence in the aging and diseased brain reveals DNA damage may play a central role in neuroinflammation associated with neurodegenerative disease.”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Bussian et al, 2018
In the citing paper
“For example both microglia (Bussian et al, 2018), astrocytes (Bussian et al, 2018), and neurons (Musi et al, 2018) have been found to display senescent‐like phenotypes in Tau P301S mice, and have been proposed as drivers of cognitive decline and neurodegeneration.”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Bussian et al, 2018
In the citing paper
“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 Bussian et al, 2018
In the citing paper
“genetic and pharmacological clearance of senescent cells confers therapeutic benefits in models of Alzheimer’s disease”
From Skeletal muscle aging, cellular senescence, and senotherapeutics: current knowledge and future directions (2021) · cites this paper as Bussian et al., 2018
In the citing paper
“They have also been identified as a putative senescent population in natural aging in both humans [42] and mice [27], mouse models of AD pathology [26], and in TBI [28,29].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [26]
In the citing paper
“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 [26]
In the citing paper
“Whole-body clearance of p16-expressing cells in a mouse model of tauopathy led to an amelioration of disease, with microglia identified as a senescent cell population in this disease model [26].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [26]
In the citing paper
“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 [26]
In the citing paper
“Senescent cells accumulate with age [23, 157, 175], neurodegenerative disease and cognitive decline [15], neuropsychiatric disorders [33], and have recently been discovered to accumulate after TBI [3, 123, 131, 132, 151].”
From Early onset senescence and cognitive impairment in a murine model of repeated mTBI (2021) · cites this paper as [15]
In the citing paper
“Similarly, accumulation of senescent glial cells drives tau pathology and cognitive decline in mice [14].”
From DNA repair deficiency and senescence in concussed professional athletes involved in contact sports (2019) · cites this paper as [14]
In the citing paper
“The role of senescent cells in cognitive decline and p-tau pathology has been demonstrated in a transgenic mouse model of AD, in which eliminating senescent cells through senolytic intervention resulted in reduced tau phosphorylation, improved cognitive outcomes, and the prevention of the upregulation of senescence genes [14].”
From DNA repair deficiency and senescence in concussed professional athletes involved in contact sports (2019) · cites this paper as [14]
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A biomarker that identifies senescent human cells in culture and in aging skin in vivo.
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Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders
Baker, D. J., Wijshake, T., Tchkonia, T., LeBrasseur, N. K., Childs, B. G., van de Sluis, B., Kirkland, J. L., & van Deursen, J. M. (2011) · Nature · doi:10.1038/nature10600 · Cited by 3,670
Self-citationNaturally occurring p16Ink4a-positive cells shorten healthy lifespan
Baker, D. J., Childs, B. G., Durik, M., Wijers, M. E., Sieben, C. J., Zhong, J., A. Saltness, R., Jeganathan, K. B., Verzosa, G. C., Pezeshki, A., et al. (2016) · Nature · doi:10.1038/nature16932 · Cited by 2,876
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Synapse Loss and Microglial Activation Precede Tangles in a P301S Tauopathy Mouse Model
Yoshiyama, Y., Higuchi, M., Zhang, B., Huang, S.-M., Iwata, N., Saido, T. C., Maeda, J., Suhara, T., Trojanowski, J. Q., & Lee, V. M.-Y. (2007) · Neuron · doi:10.1016/j.neuron.2007.01.010 · Cited by 2,208
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Metadata
- Authors
- Bussian, T. J., Aziz, A., Meyer, C. F., Swenson, B. L., van Deursen, J. M., & Baker, D. J.
- Affiliations
- Mayo Clinic (US)
- Corresponding author
- Baker, Darren J.
- Venue
- Nature
- Published
- 2018-09-19
- Volume
- 562
- Issue
- 7728
- Pages
- 578-582
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC6206507
- OpenAlex
- W2890865075
- Cited by
- 1,289
- References
- 35
- Citations by year
- 2026: 140 · 2025: 165 · 2024: 185 · 2023: 161 · 2022: 173 · 2021: 157 · 2020: 169 · 2019: 127 · 2018: 12
- FWCI
- 79.93
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- Funders
- National Institute on Aging (R01AG053229)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- cellular senescence, senolytics, astrocytes, microglia, tauopathy, neurofibrillary tangles, tau hyperphosphorylation, cognitive decline, neuronal loss, p16INK4a, gliosis, neurodegeneration
- MeSH terms
- Aniline Compounds, Animals, Astrocytes, Female, Gliosis, Humans, Male, Mice, Transgenic, Neuroglia, Phosphorylation, Solubility, Sulfonamides, Neurofibrillary Tangles, tau Proteins, Cellular Senescence, Transgenes, Cyclin-Dependent Kinase Inhibitor p16, Mice, Cognitive Dysfunction
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