The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.
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.
Overview
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
Verification
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?
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
“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
“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
“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
“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]
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
“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]
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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Fiji: an open-source platform for biological-image analysis
Schindelin, J., Arganda-Carreras, I., Frise, E., Kaynig, V., Longair, M., Pietzsch, T., Preibisch, S., Rueden, C., Saalfeld, S., Schmid, B., et al. (2012) · Nature Methods · doi:10.1038/nmeth.2019 · Cited by 66,890
The serial cultivation of human diploid cell strains
Hayflick, L., & Moorhead, P. S. (1961) · Experimental Cell Research · doi:10.1016/0014-4827(61)90192-6 · Cited by 8,508
A biomarker that identifies senescent human cells in culture and in aging skin in vivo.
Dimri, G. P., Lee, X., Basile, G., Acosta, M., Scott, G., Roskelley, C., Medrano, E. E., Linskens, M., Rubelj, I., & Pereira-Smith, O. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.20.9363 · Cited by 7,477
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
Self-citationAdult Neurogenesis in the Mammalian Brain: Significant Answers and Significant Questions
Ming, G.-L., & Song, H. (2011) · Neuron · doi:10.1016/j.neuron.2011.05.001 · Cited by 2,651
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
Clearance of senescent cells by ABT263 rejuvenates aged hematopoietic stem cells in mice
Chang, J., Wang, Y., Shao, L., Laberge, R.-M., Demaria, M., Campisi, J., Janakiraman, K., Sharpless, N. E., Ding, S., Feng, W., et al. (2016) · Nature Medicine · doi:10.1038/nm.4010 · Cited by 1,819
Jeon, O. H., Kim, C., Laberge, R.-M., Demaria, M., Rathod, S., Vasserot, A. P., Chung, J. W., Kim, D. H., Poon, Y., David, N., et al. (2017) · Nature Medicine · doi:10.1038/nm.4324 · Cited by 1,515
Self-citationSenescent cells: an emerging target for diseases of ageing
Childs, B. G., Gluscevic, M., Baker, D. J., Laberge, R.-M., Marquess, D., Dananberg, J., & van Deursen, J. M. (2017) · Nature Reviews Drug Discovery · doi:10.1038/nrd.2017.116 · Cited by 1,284
Self-citation
Cited by
Sorted by citations
Items 701–800 of 1,002
Vascular Senescence: A Potential Bridge Between Physiological Aging and Neurogenic Decline
Rojas-Vázquez, S., Blasco-Chamarro, L., López-Fabuel, I., Martínez-Máñez, R., & Fariñas, I. (2021) · Frontiers in Neuroscience · doi:10.3389/fnins.2021.666881 · Cited by 15
Exploring Autophagy Inducing Molecules: Targeting Diverse Pathways in Alzheimer's Disease Management
Singh, B., Mahajan, S., Abdella, S., Khan, R., & Garg, S. (2025) · Medicinal Research Reviews · doi:10.1002/med.70013 · Cited by 16
Human iPSC-Derived Neurons as A Platform for Deciphering the Mechanisms behind Brain Aging
Chao, C., Shen, P.-W., Tzeng, T., Kung, H., Tsai, T., & Wong, Y. (2021) · Biomedicines · doi:10.3390/biomedicines9111635 · Cited by 13
m6A methylation in cellular senescence of age-associated diseases
Gao, P., Yao, F., Pang, J., Yin, K., & Zhu, X. (2023) · Acta Biochimica et Biophysica Sinica · doi:10.3724/abbs.2023107 · Cited by 15
YAP in development and disease: Navigating the regulatory landscape from retina to brain
Zhao, Y., Sun, B., Fu, X., Zuo, Z., Qin, H., & Yao, K. (2024) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2024.116703 · Cited by 18
Wang, C., Wang, X., Sun, S., Chang, Y., Lian, P., Guo, H., Zheng, S., Ma, R., & Li, G. (2024) · Immunity & Ageing · doi:10.1186/s12979-024-00437-0 · Cited by 17
Decoding molecular mechanisms: brain aging and Alzheimer’s disease
Hayat, M., Syed, R. A., Qaiser, H., Uzair, M., Al-Regaiey, K., Khallaf, R. A., Albassam, L. A. M., Kaleem, I., Wang, X., Wang, R., et al. (2024) · Neural Regeneration Research · doi:10.4103/nrr.nrr-d-23-01403 · Cited by 14
Yassaghi, Y., Nazerian, Y., Ghasemi, M., Nazerian, A., Sayehmiri, F., Perry, G. L., & Pourbadie, H. G. (2024) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.18554 · Cited by 15
The Quest for Eternal Youth: Hallmarks of Aging and Rejuvenating Therapeutic Strategies
Nunkoo, V. S., Cristian, A., Jurcău, A., Diaconu, R. G., & Jurcău, M. C. (2024) · Biomedicines · doi:10.3390/biomedicines12112540 · Cited by 15
Jin, C., & Bhaskar, S. M. M. (2025) · European Journal of Neuroscience · doi:10.1111/ejn.70246 · Cited by 14
Cell Senescence, Telomerase, and Senolytic Therapy
Fossel, M. (2019) · OBM Geriatrics · doi:10.21926/obm.geriatr.1901034 · Cited by 14
Gu, Y., Han, J., Fan, X., Xiao, H., Chen, L., Zhao, Z., & Zhang, Y. (2022) · Food & Function · doi:10.1039/d1fo04130d · Cited by 14
Tun, X., Wang, E. J., Gao, Z., Lundberg, K. C., Xu, R., & Hu, D. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24065697 · Cited by 14
Spatial cell type mapping of multiple sclerosis lesionsPreprint
Lerma-Martin, C., Badia-i-Mompel, P., Flores, R. O. R., Sekol, P., Hofmann, A., Thäwel, T., Riedl, C. J., Wünnemann, F., Ibarra-Arellano, M. A., Trobisch, T., et al. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.11.03.514906 · Cited by 14
Yang, W., Fang, J., Zhai, J., Qiu, C., Liang, Z., Liu, Q., & Wei, H. (2024) · BMC Medicine · doi:10.1186/s12916-024-03609-3 · Cited by 15
Stromal senescence contributes to age-related increases in cancer
Ye, J., Melam, A., & Stewart, S. A. (2025) · Nature reviews. Cancer · doi:10.1038/s41568-025-00840-9 · Cited by 16
Tsang, V. S. K., Malaspina, A., & Henson, S. M. (2025) · Journal of Inflammation · doi:10.1186/s12950-025-00460-y · Cited by 14
Zhuo, Y., Yao, L., Zhu, Y., Wen, N., Zou, G.-J., Lu, H., Pei, X., Zhang, Y., Zhang, Q., Wang, X., et al. (2025) · Nature Biomedical Engineering · doi:10.1038/s41551-025-01525-2 · Cited by 15
Fluorescence lifetime clocks quantify senescence and aging
Yan, C., Liu, C., Liu, B., Zheng, Q., Zhao, X., Lu, S., Fu, X., Li, W., Li, J., Li, D., et al. (2025) · Nature Aging · doi:10.1038/s43587-025-01001-1 · Cited by 15
Cellular Senescence in Liver Cancer: How Dying Cells Become “Zombie” Enemies
Gazzillo, A., Volponi, C., Soldani, C., Polidoro, M. A., Franceschini, B., Lleò, A., Bonavita, E., & Donadon, M. (2023) · Biomedicines · doi:10.3390/biomedicines12010026 · Cited by 14
Regulation of cellular senescence by innate immunity
Hou, J., Zheng, Y., & Gao, C. (2023) · Biophysics Reports · doi:10.52601/bpr.2023.230032 · Cited by 17
Xia, W., Chen, H., Han, Y., Zhu, L.-X., Xie, C., & Hou, M. (2024) · FEBS Journal · doi:10.1111/febs.17164 · Cited by 14
From bench to bedside: The critical need for standardized senescence detection
Shah, J., Al-Hashimi, A., Benedetto, M., & Ruchaya, P. J. (2025) · Archives of cardiovascular diseases · doi:10.1016/j.acvd.2024.12.008 · Cited by 13
Sex, senescence, senolytics, and cognition
Foster, T. C., & Kumar, A. (2025) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2025.1555872 · Cited by 15
Rejuvenation of Senescent Cells, In Vitro and In Vivo, by Low‐Frequency Ultrasound
Kureel, S. K., Maroto, R., Aniqua, M., Powell, S. N., Singh, E., Margadant, F., Blair, B., Rasmussen, B. B., & Sheetz, M. P. (2025) · Aging Cell · doi:10.1111/acel.70008 · Cited by 13
Enhanced xeno-free differentiation of hiPSC-derived astroglia applied in a blood–brain barrier model
Delsing, L., Kallur, T., Zetterberg, H., Hicks, R., & Synnergren, J. (2019) · Fluids and Barriers of the CNS · doi:10.1186/s12987-019-0147-4 · Cited by 13
The eroding chromatin landscape of aging stem cells
Shi, C., Wang, L., & Sen, P. (2020) · Translational Medicine of Aging · doi:10.1016/j.tma.2020.08.002 · Cited by 14
Pham, D., Polgár, B., Toth, T., Jüngling, A., Kovács, N., Balás, I., Pál, E., Szabo, D., Fulop, B. D., Reglődi, D., et al. (2022) · GeroScience · doi:10.1007/s11357-022-00530-6 · Cited by 16
A novel prognostic model based on cellular senescence-related gene signature for bladder cancer
Luo, L., Li, F., Gong, B., Xi, P., & Xie, W. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.937951 · Cited by 13
Wu, C., & Feng, Y. (2023) · Frontiers in Neuroscience · doi:10.3389/fnins.2023.1097067 · Cited by 16
Regulation of cellular senescence by retinoid X receptors and their partners
Martin, N., Ma, X., & Bernard, D. (2019) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2019.111131 · Cited by 13
Yang, Y., Duan, C., Huang, L., Xia, X., Zhong, Z., Wang, B., Wang, Y., & Ding, W. (2020) · Behavioural Brain Research · doi:10.1016/j.bbr.2020.112838 · Cited by 13
Breast cancer type 1 and neurodegeneration: consequences of deficient DNA repair
Leung, E., & Hazrati, L. (2021) · Brain Communications · doi:10.1093/braincomms/fcab117 · Cited by 14
Connections Between Cellular Senescence and Alzheimer’s Disease—A Narrative Review
Kuźniar, J., Kozubek, P., Czaja, M., Sitka, H., Kochman, U., & Leszek, J. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26178638 · Cited by 14
Senescent Astrocytes: A New Player in Brain Aging and Cognitive Decline
Pessoa, B., Hayashide, L. D. S., Dias, G. R., Pontes, B., Pinto, R. S., & Diniz, L. P. (2026) · Brain Sciences · doi:10.3390/brainsci16010076 · Cited by 13
Telomerase and neurons: an unusual relationship
Saretzki, G. C. (2022) · Neural Regeneration Research · doi:10.4103/1673-5374.336133 · Cited by 12
Immunosenescence of brain accelerates Alzheimer’s disease progression
Chen, H.-Y., Zhao, Y. G., & Xie, Y. (2022) · Reviews in the Neurosciences · doi:10.1515/revneuro-2022-0021 · Cited by 12
Gao, Y., Xu, L., Li, Y., Qi, D., Wang, C., Luan, C., Zheng, S., Du, Q., Liu, W., Lu, G., et al. (2024) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2024.111902 · Cited by 12
Seol, S.-I., Davaanyam, D., Oh, S.-A., Lee, E. H., Han, P., Kim, S., & Lee, J.-K. (2024) · Cells · doi:10.3390/cells13020189 · Cited by 15
Pumo, A., & Legeay, S. (2024) · Brain Research · doi:10.1016/j.brainres.2024.148817 · Cited by 14
Fibroblast senescence-associated extracellular matrix promotes heterogeneous lung niche
Howes, A. M., Dea, N. C., Ghosh, D., Krishna, K., Wang, Y., Li, Y., Morrison, B., Toussaint, K. C., & Dawson, M. (2024) · APL Bioengineering · doi:10.1063/5.0204393 · Cited by 12
Liu, D., Hsueh, S., Tweedie, D., Price, N., Glotfelty, E. J., Lecca, D., Telljohann, R. S., de Cabo, R., Hoffer, B. J., & Greig, N. H. (2024) · Brain Communications · doi:10.1093/braincomms/fcae204 · Cited by 13
Sun, H., Gao, X., Niu, J., Chen, P., He, S., Xu, S., & Ge, J. (2024) · eneuro · doi:10.1523/eneuro.0310-24.2024 · Cited by 12
Mielke, M. M., Fielding, R. A., Atkinson, E. J., Aversa, Z., Schafer, M. J., Cummings, S. R., Pahor, M., Leeuwenburgh, C., & LeBrasseur, N. K. (2025) · The journal of nutrition health & aging · doi:10.1016/j.jnha.2025.100529 · Cited by 13
The Effects of IL-1β on Astrocytes are Conveyed by Extracellular Vesicles and Influenced by Age
Willis, C. M., Sutter, P. A., Rouillard, M. E., & Crocker, S. J. (2020) · Neurochemical Research · doi:10.1007/s11064-019-02937-8 · Cited by 12
A Senolytic-Eluting Coronary Stent for the Prevention of In-Stent Restenosis
Kim, C., Lee, S.-G., Lim, S., Jung, M., Kwon, S. P., Hong, J., Kang, M., Sohn, H. S., Go, S., Moon, S., et al. (2022) · ACS Biomaterials Science & Engineering · doi:10.1021/acsbiomaterials.1c01611 · Cited by 12
Ding, J., Dai, Y., Zhu, J., Fan, X., Zhang, H., & Tang, B. (2022) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2022.1050837 · Cited by 12
Navitoclax improves acute‐on‐chronic liver failure by eliminating senescent cells in mice
Watanabe, Y., Abé, H., Kimura, N., Arao, Y., Ishikawa, N., Yuichiro, M., Setsu, T., Sakamaki, A., Kamimura, H., Yokoo, T., et al. (2023) · Hepatology Research · doi:10.1111/hepr.13879 · Cited by 12
Doan, L., Paine, P., Tran, C., Parsons, B., Hiller, A., Joshua, I., Collaco, N., Vitari, A., de Morrée, A., Ishak, H. D., et al. (2020) · doi:10.21203/rs.3.rs-92962/v1 · Cited by 14
Exploring aging interventions in human brain organoids
Aguado, J., & Wolvetang, E. J. (2022) · Aging · doi:10.18632/aging.203925 · Cited by 12
Current aspects of targeting cellular senescence for the therapy of neurodegenerative diseases
Jaganathan, R., Iyaswamy, A., Krishnamoorthi, S., Thakur, A., Durairajan, S. S. K., Yang, C., & Wankhar, D. (2025) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2025.1627921 · Cited by 12
Cáceres-Palomo, L., Sánchez‐Mejías, E., Trujillo‐Estrada, L., Pérez-Moreno, J. J., Lopez-Oliva, E., Lim, T. E., DeFlitch, L., Chang, S. H., Kampman, L., Corces, M. R., et al. (2025) · Journal of Neuroinflammation · doi:10.1186/s12974-025-03607-z · Cited by 11
Wang, L., Bukhari, H., Kong, L., Hagemann, T. L., Zhang, S.-C., Messing, A., & Feany, M. Β. (2022) · Journal of Neuroscience · doi:10.1523/jneurosci.1659-21.2021 · Cited by 11
BAY 11-7082 inhibits the secretion of interleukin-6 by senescent human microglia
Cook, M., Lin, H., Mishra, S. K., & Wang, G. Y. (2022) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2022.05.090 · Cited by 11
Mein, H., Yu, J., Ahmad, F., Zhang, H., & Liu, P. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23116039 · Cited by 11
Huang, Z. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-221042 · Cited by 12
Ruan, Y., Lv, W., Li, S., Cheng, Y., Wang, D., Zhang, C., & Shimizu, K. (2023) · Computers in Biology and Medicine · doi:10.1016/j.compbiomed.2023.106922 · Cited by 11
Ganoderic Acid A: A Potential Natural Neuroprotective Agent for Neurological Disorders: A Review
Ma, F., Wang, J., Jiang, W., Luo, J., Yang, R., Zhang, L., & Han, C. (2023) · International journal of medicinal mushrooms · doi:10.1615/intjmedmushrooms.2023051918 · Cited by 11
Role of long noncoding RNA in regulating HIV infection—a comprehensive review
Amir, N., & Taube, R. (2024) · mBio · doi:10.1128/mbio.01925-23 · Cited by 11
The caspase-activated DNase promotes cellular senescence
Haimovici, A., Rupp, V., Amer, T., Moeed, A., Weber, A., & Häcker, G. A. (2024) · The EMBO Journal · doi:10.1038/s44318-024-00163-9 · Cited by 11
Amyloid-β-activated microglia can induce compound proteinopathies
Lee, S. H., Bae, E.-J., Pérez-Acuña, D., Jung, M. K., Han, J. W., Mook‐Jung, I., & Lee, S. (2024) · Brain · doi:10.1093/brain/awae221 · Cited by 11
Dziewa, M., Złotek, M., Herbet, M., & Piątkowska‐Chmiel, I. (2024) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-024-01514-0 · Cited by 11
Weng, W., Lin, B., Zheng, J., Sun, Y., Li, Z., Chen, X., Wang, Y., & Pan, X. (2025) · Phytomedicine · doi:10.1016/j.phymed.2025.156502 · Cited by 12
Lambert, M., Miquel, G., Villeneuve, L. R., Thorin‐Trescases, N., & Thorin, É. (2025) · GeroScience · doi:10.1007/s11357-025-01563-3 · Cited by 11
Aging-dependent YAP1 reduction contributes to AD pathology by upregulating the Nr4a1-AKT/GSK-3β axis
Lei, L., Cheng, Y., Yin, A., Han, J.-M., Wu, G., Yang, F., Wang, Q., Wang, J., Liu, R., Li, H., et al. (2025) · Translational Neurodegeneration · doi:10.1186/s40035-025-00487-4 · Cited by 13
Bigan, E., Nair, S. S., Lejeune, F., Fragnaud, H., Parmentier, F., Mégret, L., Verny, M., Aaronson, J., Rosinski, J., & Néri, C. (2019) · Bioinformatics · doi:10.1093/bioinformatics/btz514 · Cited by 12
Review of DNA repair enzymes in bacteria: With a major focus on AddAB and RecBCD
Wang, B., Xu, J.-Z., Zhang, F., Liu, S., Liu, J., & Zhang, W. (2022) · DNA repair · doi:10.1016/j.dnarep.2022.103389 · Cited by 12
Okamura, K., Suzuki, T., & Nohara, K. (2020) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2020.115259 · Cited by 11
Gu, J. (2025) · American Journal of Cancer Research · doi:10.62347/atcd4291 · Cited by 11
He, Z., Zhang, H., Li, X., Tu, S., Wang, Z., Han, S., Du, X., Shen, L., Li, N., & Liu, Q. (2022) · Phytomedicine · doi:10.1016/j.phymed.2022.154555 · Cited by 12
Role of Senescence and Neuroprotective Effects of Telomerase in Neurodegenerative Diseases
Ding, X., Liu, X., Wang, F., Wang, F., & Geng, X. (2019) · Rejuvenation Research · doi:10.1089/rej.2018.2115 · Cited by 12
Blunting senescence boosts liver regenerationPreprint
Birch, J., & Gil, J. (2020) · Genes & Development · doi:10.1101/gad.337394.120 · Cited by 11
Immunosenescence: Molecular Mechanisms, Diseases, and Therapeutic Innovations
Gong, N., Pan, X., Deng, Y., Che, J., Bao, J., Wang, M., Xu, C., Liu, X., & Shi, Y. (2025) · MedComm · doi:10.1002/mco2.70515 · Cited by 14
Basic Microglial Functions and How They Go Awry in Neurodegenerative Disease
McKinney, J. E., Bennett, M. L., & Bennett, F. C. (2026) · Annual Review of Pathology Mechanisms of Disease · doi:10.1146/annurev-pathmechdis-042624-114332 · Cited by 13
Suk, K. (2026) · Experimental Neurology · doi:10.1016/j.expneurol.2026.115737 · Cited by 11
The intersection between toxicology and aging research: A toxic aging coin perspective
Wise, J. P. (2022) · Frontiers in Aging · doi:10.3389/fragi.2022.1014675 · Cited by 12
Chronic inflammation: a potential target in tauopathies
Ising, C., & Heneka, M. T. (2023) · The Lancet Neurology · doi:10.1016/s1474-4422(23)00116-3 · Cited by 10
de Celis, M. F. R., & Bonner‐Weir, S. (2023) · Frontiers in Endocrinology · doi:10.3389/fendo.2023.1217729 · Cited by 11
Activated microglia release β−galactosidase that promotes inflammatory neurodegeneration
Kitchener, E. J. A., Dundee, J. M., & Brown, G. C. (2024) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2023.1327756 · Cited by 10
Chen, X., Walton, K. L., Brodaty, H., & Chalton, K. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-231222 · Cited by 10
Cholesterol Accumulation Promotes Photoreceptor Senescence and Retinal Degeneration
Terao, R., Sohn, B. S., Yamamoto, T., Lee, T. J., Colasanti, J. J., Pfeifer, C. W., Lin, J. B., Santeford, A. C., Yamaguchi, S., Yoshida, M., et al. (2024) · Investigative Ophthalmology & Visual Science · doi:10.1167/iovs.65.10.29 · Cited by 11
The putative contribution of cellular senescence to driving tauopathies
Karabag, D., Heneka, M. T., & Ising, C. (2024) · Trends in Immunology · doi:10.1016/j.it.2024.08.006 · Cited by 11
SenMayo transcriptomic senescence panel highlights glial cells in the ageing mouse and human retina
Suresh, S., Karthik, G., Ouyang, J. F., Chrysostomou, V., Tang, S. A., Petretto, E. G., Crowston, J. G., & Bell, K. C. (2024) · npj Aging · doi:10.1038/s41514-024-00187-9 · Cited by 10
Wang, Y., Zou, H., Dong, Z., Shi, W., Huang, J., Yang, M., Xiang, X., Xiaotong, L., Zhifeng, L., Wang, G., et al. (2025) · Biomaterials · doi:10.1016/j.biomaterials.2025.123312 · Cited by 10
Manavi, Z., Melchor, G. S., Bullard, M. R., Gross, P. S., Ray, S., Gaur, P., Baydyuk, M., & Huang, J. K. (2025) · Journal of Neuroinflammation · doi:10.1186/s12974-025-03425-3 · Cited by 10
Wu, J., Zhang, L., Zhao, Z., Liu, Y., Li, Z., Feng, X., Zhang, L., Yao, X., Du, J., Chen, L., et al. (2025) · Ageing Research Reviews · doi:10.1016/j.arr.2025.102783 · Cited by 10
Gu, C., Guo, T., Chen, X., Zhou, X., & Sun, Y. (2025) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-025-01580-y · Cited by 11
A human neuron Alzheimer’s disease model reveals barriers to senolytic translatability
Walton, C. C., Wang, E. Y., Lee, S., Siebrand, C. J., Bergo, N. J., Mayeri, Z., & Andersen, J. K. (2025) · Alzheimer s Research & Therapy · doi:10.1186/s13195-025-01822-7 · Cited by 10
Tau aggregation and its relation to selected forms of neuronal cell death
Tolkovsky, A. M., & Spillantini, M. G. (2021) · Essays in Biochemistry · doi:10.1042/ebc20210030 · Cited by 13
Microglia: Rheostats of space radiation effects in the CNS microenvironment
Kerry O'Banion, M. (2022) · Life Sciences in Space Research · doi:10.1016/j.lssr.2022.08.002 · Cited by 10
Roles of Microglia in AD Pathology
Gao, R., Wu, H., Li, Q., & Zhao, J. (2023) · Current Alzheimer Research · doi:10.2174/1567205020666230203112351 · Cited by 10
Tshilenge, K., Bons, J., Aguirre, C. G., Gerónimo‐Olvera, C., Shah, S., Rose, J., Gerencser, A. A., Mak, S. K., Ehrlich, M. E., Bragg, D. C., et al. (2023) · Neurobiology of Disease · doi:10.1016/j.nbd.2023.106367 · Cited by 10
Chen, P., Wang, Y., & Zhou, B. (2024) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2024.111918 · Cited by 10
Anti-Aβ antibodies bound to neuritic plaques enhance microglia activity and mitigate tau pathology
Laversenne, V., Nazeeruddin, S., Källstig, E., Colin, P., Voize, C., & Schneider, B. L. (2020) · Acta Neuropathologica Communications · doi:10.1186/s40478-020-01069-3 · Cited by 11
Involvement of astrocyte senescence in Alzheimer's disease
Tüzer, F., & Torres, C. A. (2022) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2022.102594 · Cited by 10
Senescent cells in the development of cardiometabolic disease
Postmus, A. C., Sturmlechner, I., Jonker, J. W., van Deursen, J. M., van de Sluis, B., & Kruit, J. K. (2019) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000602 · Cited by 10
Cellular senescence in neurodegenerative diseases
Zhang, P., & Sung, M. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-822514-1.00012-2 · Cited by 10
Jin, M., Xu, R., Alam, M. M., Ma, Z., Zhu, S., Wang, L., Martini, A. C., Bernabucci, M., Xie, P., Kwan, K. Y., et al. (2021) · SSRN Electronic Journal · doi:10.2139/ssrn.3985173 · Cited by 10
Senolytic CAR T cells reverse aging-associated defects in intestinal regeneration and fitnessPreprint
Eskiocak, O., Chowdhury, S., Shah, V., Nnuji-John, E., Chung, C., Boyer, J. A., Harris, A. S., Habel, J., Sadelain, M., Beyaz, S., et al. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.03.19.585779 · Cited by 10
Caloric Restriction Improves Spatial Learning Deficits in Tau Mice
Cogut, V., McNeely, T. L., Bussian, T. J., Graves, S. I., & Baker, D. J. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-231117 · Cited by 10
Self-citation
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
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
