The DOI matches its Crossref record; 101 of the 102 references it cites were found in a registry or an index; none of the 43 sources its claims cite is checked for support yet.
Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives
Open accessAbstract
Along with a general decline in overall health, most chronic degenerative human diseases are inherently associated with increasing age. Age-associated cognitive impairments and neurodegenerative diseases, such as Parkinson's and Alzheimer's diseases, are potentially debilitating conditions that lack viable options for treatment, resulting in a tremendous economic and societal cost. Most high-profile clinical trials for neurodegenerative diseases have led to inefficacious results, suggesting that novel approaches to treating these pathologies are needed. Numerous recent studies have demonstrated that senescent cells, which are characterized by sustained cell cycle arrest and production of a distinct senescence-associated secretory phenotype, accumulate with age and at sites of age-related diseases throughout the body, where they actively promote tissue deterioration. Cells with features of senescence have been detected in the context of brain aging and neurodegenerative disease, suggesting that they may also promote dysfunction. Here, we discuss the evidence implicating senescent cells in neurodegenerative diseases, the mechanistic contribution of these cells that may actively drive neurodegeneration, and how these cells or their effects may be targeted therapeutically.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
0 of 43 cited sources checked · 0 supported · 0 flagged
In the paper
“Recent work has demonstrated that senescent cells, characterized by an arrested cell cycle that is triggered by a variety of stresses, accumulate in various tissues of age and disease (4)(5)(6)(7)(8)”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Introduction
What the sources say
- Not checked yetcites (4)(5)(6)(7)(8)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“Just like in peripheral tissues, aging leads to a chronic low-grade inflammation in the brain (42), which occurs in the absence of any obvious pathogen.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Evidence for senescence in the CNS
What the sources say
- Not checked yetcites [42] Frank-Cannon, 2009, Does neuroinflammation fan the flame in neurodegenerative diseases?, Mol Neurodegener source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“As these markers are not truly unique to senescent cells, it is imperative to establish that these changes occur in the context of senescence and not just as a result of inflammation, for example.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Evidence for senescence in CNS aging and disease
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“With age, human brain tissue displays an increase in the number of astrocytes positive for p16 INK4A and matrix metalloproteinase 3 (MMP3) (57), a common SASP-associated protease.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > mation.
What the sources say
- Not checked yetcites [57] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“Microglia from aged mice exhibit increased production of the proinflammatory cytokines IL-6, IL-1β, and TNF-α (48, 49), all of which are factors upregulated in senescent cells (9).”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Microglia.
What the sources say
- Not checked yetcites [48] source
- Not checked yetcites [49] Bachstetter, 2011, Microglial p38α MAPK is a key regulator of proinflammatory cytokine up-regulation induced by toll-like receptor (TLR) ligands or beta-amyloid (Aβ), J Neuroinflammation source
- Not checked yetcites [9] Coppé, 2008, Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor, PLoS Biol source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“For example, microglia from AD patients possess shorter telomeres compared with age-matched controls (50).”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > R E V I E W S E R I E S : C E L L U L A R S E N E S C E N C E I N H U M A N D I S E A S E
What the sources say
- Not checked yetcites [50] source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Telomere attrition is inherently linked to proliferation; therefore this process is unlikely to occur in postmitotic cells, such as neurons and oligodendrocytes, under normal circumstances.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Evidence for senescence in the CNS
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“Indeed, treating primary astrocytes in vitro with these drugs promotes senescence (87,88).”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Other neurodegenerative conditions.
What the sources say
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Current methods rely on a combination of markers, including those described in Figure 1.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Evidence for senescence in CNS aging and disease
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“Astrocytes cultured from patients with AD express not only more of the CDKi p16 INK4A than age-matched controls, but also more MMP1 and IL-6 (57).”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > R E V I E W S E R I E S : C E L L U L A R S E N E S C E N C E I N H U M A N D I S E A S E
What the sources say
- Not checked yetcites [57] source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes
- It may state two separate claims as one. 20
- Probably not a substantial claim. 5
In the paper
“Subsequent studies using the INK-ATTAC model determined that senescent cells drive various natural age-related pathologies, shorten life, and promote the age-associated diseases atherosclerosis and osteoarthritis (20,(29)(30)(31).”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > mation.
What the sources say
- Not checked yetcites (20,(29)(30)(31)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Importantly, p16 INK4A is a biomarker of natural aging, as its expression increases in a variety of tissues with time (28).”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Properties of senescent cells
What the sources say
- Not checked yetcites [28] source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“This contributes to decreased pre-and postsynaptic densities, as well as decreased synapses and dendritic spines overall (43), resulting in cognitive impairments and memory loss in aged individuals.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Evidence for senescence in the CNS
What the sources say
- Not checked yetcites [43] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Studies have demonstrated that neurons of aged mice accumulate high amounts of DNA damage (16) and display elevated expression of proinflammatory molecules and SA β-gal activity (41), characteristics typical of senescence.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > mation.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“It is important to note that while these changes are indicative of senescence, there is currently no single marker that can be used independently to define a senescent cell.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > mation.
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Unlike a normally programmed terminal differentiation process, senescence is a distinct proinflammatory fate in which cells acquire a distinctive secretome of cytokines, chemokines, proteases, and growth factors collectively known as the senescence-associated secretory phenotype (SASP) (9).”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Introduction
What the sources say
- Not checked yetcites [9] Coppé, 2008, Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor, PLoS Biol source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
In the paper
“BUBR1 hypomorphic mice display leakage across the BBB that correlates with a propensity for neural endothelial cells and pericytes to prematurely senesce, become SA β-gal positive, and express p16 INK4A (66).”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Other neurodegenerative conditions.
What the sources say
- Not checked yetcites [66] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The above studies suggest that senescent cells may accumulate with age and at sites of pathology in the brain.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Evidence for senescence in CNS aging and disease
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“One limitation of genetic inactivation experiments is that mice lacking p16 INK4A are highly tumor prone and therefore die before the cognitive decline is observed in normal mice (90).”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Evidence for senescence in CNS aging and disease
What the sources say
- Not checked yetcites [90] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Interestingly, a common feature of PD patients and mouse models is the accumulation of activated microglia and astrocytes, which would promote increased local concentrations of inflammatory mediators and ROS (84).”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > R E V I E W S E R I E S : C E L L U L A R S E N E S C E N C E I N H U M A N D I S E A S E
What the sources say
- Not checked yetcites [84] source
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A true demonstration that senescent cells causally drive neuropathology can be achieved either by prevention of senescence entry through genetic inactivation of p16 INK4A or by direct elimination of senescent cells using genetically engineered mice.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Evidence for senescence in CNS aging and disease
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Navitoclax treatment has been shown to eliminate senescent cells that arise in early atherosclerotic plaques (30) and upon sublethal irradiation in both skeletal muscle and the bone marrow (93).”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Evidence for senescence in CNS aging and disease
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The finding that senescent cell elimination is not only possible but also effective at modulating inflammatory diseases has triggered profound interest in developing therapeutic strategies to eliminate senescent cells in the absence of genetic modifications.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Evidence for senescence in CNS aging and disease
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“When ganciclovir is administered, HSV-TK converts this compound into a toxic DNA chain terminator in p16 INK4A -expressing cells, triggering apoptosis in senescent cells through mitochondria-dependent cell death (92).”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Evidence for senescence in CNS aging and disease
What the sources say
- Not checked yetcites [92] Laberge, 2013, Mitochondrial DNA damage induces apoptosis in senescent cells, Cell Death Dis source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“These “senolytic” approaches eliminate not only the senescent cell but also the accompanying SASP, which likely exerts beneficial effects in the local environment where senescent cells reside.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Evidence for senescence in CNS aging and disease
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The senolytic molecules ABT-737 (37) and navitoclax (ABT-263) (93) occupy the inhibitory binding regions of members of the BCL-2 family of proteins, thereby canceling their antiapoptotic activity.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Evidence for senescence in CNS aging and disease
What the sources say
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The BBB may preclude systemic administration for some of these compounds to get to the target site.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Evidence for senescence in CNS aging and disease
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The aforementioned studies demonstrate a beneficial role for senescence in tissue repair and remodeling in the short term, whereas the long-term consequences appear to be largely detrimental.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Evidence for senescence in CNS aging and disease
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, if these approaches are to be implemented in neurological conditions, there are likely a number of candidates that demonstrate bioavailability in the brain, in the context of both aging and disease.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Evidence for senescence in CNS aging and disease
Load-bearingStrength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Furthermore, the duration of treatments has been brief with relatively short follow-up assessments, so long-term negative consequences have not been observed in studies to date.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Evidence for senescence in CNS aging and disease
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“It is important to keep in mind that the animals used in this study were in a controlled environment without any exogenous stresses applied.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Evidence for senescence in CNS aging and disease
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Once they have entered into this state, a number of distinguishing qualities can be observed.depending on the cell type and senescence-inducing stimuli.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Outlook
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“A number of stressors, both intrinsic and extrinsic, can stimulate the conversion of otherwise normal cells into senescent cells.”
§ Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives > Outlook
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
The risk of developing neurodegenerative diseases increases dramatically with age.
“The risk of developing many pathological conditions, including neurodegenerative diseases, increases dramatically with age.”
The paper relies on this without support.
None of the numerous clinical trials to treat Alzheimer's disease have demonstrated a beneficial impact for patients.
“Unfortunately, of the numerous clinical trials to treat AD, none have been able to demonstrate beneficial impact for patients.”
The paper relies on this without support.
The role of senescent cells in causing and worsening neurodegenerative disorders remains unknown.
“However, the significance of senescent cells in both the induction and exacerbation of neurodegenerative disorders is unknown.”
The paper relies on this without support.
Determining the overall importance and mechanism of senescent cells in neuropathology has been very hard because tools to identify, isolate, or remove these cells are lacking.
“To date, it has been extremely difficult to discern the overall significance and mechanistic contribution of senescent cells to neuropathology because of a lack of tools to identify, isolate, and/or eliminate these cells.”
The paper relies on this without support.
These methods have not yet been used in relevant neurodegenerative disease studies.
“To date, these approaches have not been employed for relevant studies of neurodegenerative disease.”
The paper relies on this without support.
Whether and how senolytics can be translated into clinical practice is currently unclear.
“It is currently unclear how these various senolytics can be translated into clinical strategies, if at all.”
The paper relies on this without support.
No reliable method currently exists to detect the early signs of neurodegenerative diseases.
“as there is currently no reliable way to identify the early signs of these devastating diseases.”
The paper relies on this without support.
The molecular features that accompany normal aging and CNS disease remain incompletely characterized.
“The molecular correlates of normal aging and CNS disease are not fully defined.”
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
“Senescent cells contribute to aging and age-related pathologies21,22,23 through their senescence-associated secretory phenotype (SASP).24,25,26”
From Uncovering the signatures of aging and senescence in the human dorsolateral prefrontal cortex (2026) · cites this paper as [22]
Experimental — accuracy not yet measuredIn the citing paper
“Cellular senescence is yet another factor that can augment glial function and accelerate brain aging.”
From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [167]
In the citing paper
“Microglia, astrocytes, brain endothelial cells, and other CNS cell types show evidence of senescence and increased expression of senescence factors (167, 168).”
From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [167]
In the citing paper
“Among these aging hallmarks, cellular senescence plays a crucial role in brain aging, neurodegeneration, and dementia 36 through the SASP, which represents a major source of inflammation. 37”
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 [36]
In the citing paper
“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 [28]
In the citing paper
“Senescent cells accumulate with advancing age throughout multiple organ systems, including the brain (17, 28).”
From Senolytic Therapy to Modulate the Progression of Alzheimer's Disease (SToMP-AD): A Pilot Clinical Trial (2022) · cites this paper as [28]
In the citing paper
“Microglia and astrocytes can acquire a senescent phenotype themselves (28, 31, 32), promoting further diffusion of the SASP and the conversion of healthy cells to the senescent phenotype.”
From Senolytic Therapy to Modulate the Progression of Alzheimer's Disease (SToMP-AD): A Pilot Clinical Trial (2022) · cites this paper as [28]
In the citing paper
“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 [28]
In the citing paper
“In this regard, cellular senescence emerges as a key biological process linked to aging that can contribute to or cause the appearance of age-related pathologies like AD [5].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [5]
In the citing paper
“Indeed, markers of cellular senescence have been found in those cell types in the context of aging and neurodegenerative diseases [5].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [5]
In the citing paper
“It has been demonstrated that a variety of stressors, including oncogenic activation, reactive oxygen species (ROS) and mitochondrial dysfunction, can stimulate the conversion into a state of senescence, mostly through the generation of DNA damage [5].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [5]
In the citing paper
“Studies have demonstrated the presence of senescent cells in the brains of AD patients and mouse models [5]”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [5]
In the citing paper
“Senescent cells produce a distinct inflammatory secretome and have been found to accumulate with age and in many diseases; potentially contributing to pathology [17–21].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [20]
In the citing paper
“Senescent cells produce a distinct inflammatory secretome and have been found to accumulate with age and in many diseases; potentially contributing to pathology [17–21].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [20]
Citations
Cites
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
The limited in vitro lifetime of human diploid cell strains
Hayflick, L. (1965) · Experimental Cell Research · doi:10.1016/0014-4827(65)90211-9 · Cited by 5,876
Astrocyte-endothelial interactions at the blood-brain barrier
Abbott, N. J., Rönnbäck, L., & Hansson, E. (2006) · Nature Reviews Neuroscience · doi:10.1038/nrn1824 · Cited by 5,595
Fate Mapping Analysis Reveals That Adult Microglia Derive from Primitive Macrophages
Ginhoux, F., Greter, M., Leboeuf, M., Nandi, S., See, P., Gokhan, S., Mehler, M. F., Conway, S. J., Ng, L. G., Stanley, E. R., et al. (2010) · Science · doi:10.1126/science.1194637 · Cited by 5,175
Extension of Life-Span by Introduction of Telomerase into Normal Human Cells
Bodnar, A. G., Ouellette, M., Frolkis, M., Holt, S. E., Chiu, C.-P., Morin, G. B., Harley, C. B., Shay, J. W., Lichtsteiner, S., & Wright, W. E. (1998) · Science · doi:10.1126/science.279.5349.349 · Cited by 4,975
Cellular senescence: when bad things happen to good cells
Campisi, J., & d'Adda di Fagagna, F. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2233 · Cited by 4,441
Hearing loss and cognitive decline in older adults
Lin, F. R., Yaffe, K., Xia, J., Xue, Q.-L., Harris, T. B., Purchase-Helzner, E., Satterfield, S., Ayonayon, H. N., Ferrucci, L., Simonsick, E. M., et al. (2013) · JAMA Internal Medicine · doi:10.1001/jamainternmed.2013.1868 · Cited by 4,017
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 · cited 5×
“…into a nonproliferating cell (e.g., neurons) are capable of acquir-the control of a senescent cell–specific portion of the p16 INK4A promoter (encompassing 2.6 kb) that initiates apoptosis by dimerizing and activating the caspase-8 fusion proteins when AP20187 is administered to mice (29).”
InfluentialSelf-citationNeurovascular pathways to neurodegeneration in Alzheimer’s disease and other disorders
Zlokovic, B. V. (2011) · Nature Reviews Neuroscience · doi:10.1038/nrn3114 · Cited by 2,969
Naturally 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-citationCellular senescence: from physiology to pathology
Muñoz-Espín, D., & Serrano, M. (2014) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3823 · Cited by 2,818
Alzheimer disease in the United States (2010–2050) estimated using the 2010 census
Hebert, L. E., Weuve, J., Scherr, P. A., & Evans, D. A. (2013) · Neurology · doi:10.1212/wnl.0b013e31828726f5 · Cited by 2,642
The role of senescent cells in ageing
van Deursen, J. M. (2014) · Nature · doi:10.1038/nature13193 · Cited by 2,623
The Achilles' heel of senescent cells: from transcriptome to senolytic drugs
Zhu, Y., Tchkonia, T., Pirtskhalava, T., Gower, A. C., Ding, H., Giorgadze, N., Palmer, A. K., Ikeno, Y., Hubbard, G. B., Lenburg, M., et al. (2015) · Aging Cell · doi:10.1111/acel.12344 · Cited by 2,584 · cited 1×
“Other potentially senolytic molecules and strategies, including piperlongumine (94), dasatinib (95), quercetin (95), the proprietary compound UBX0101 (31), a FOXO4 peptide that promotes p53-dependent apoptosis (96), and HSP90 inhibitors (97), have also been identified, demonstrating that there are…”
Tripartite synapses: glia, the unacknowledged partner
Araque, A., Parpura, V., Sanzgiri, R. P., & Haydon, P. G. (1999) · Trends in Neurosciences · doi:10.1016/s0166-2236(98)01349-6 · Cited by 2,529
Oxidative stress shortens telomeres
von Zglinicki, T. (2002) · Trends in Biochemical Sciences · doi:10.1016/s0968-0004(02)02110-2 · Cited by 2,524
Heaton, R. K., Clifford, D. B., Franklin, D. R., Woods, S. P., Ake, C., Vaida, F., Ellis, R. J., Letendre, S. L., Marcotte, T. D., Atkinson, J. H., et al. (2010) · Neurology · doi:10.1212/wnl.0b013e318200d727 · Cited by 2,353
Telomere Shortening and Tumor Formation by Mouse Cells Lacking Telomerase RNA
Blasco, M. A., Lee, H.-W., Hande, M. P., Samper, E., Lansdorp, P. M., DePinho, R. A., & Greider, C. W. (1997) · Cell · doi:10.1016/s0092-8674(01)80006-4 · Cited by 2,108
Blood-brain barrier breakdown in the aging human hippocampus
Montagne, A., Barnes, S. R., Sweeney, M. D., Halliday, M. R., Sagare, A. P., Zhao, Z., Toga, A. W., Jacobs, R. E., Liu, C. Y., Amezcua, L., et al. (2015) · Neuron · doi:10.1016/j.neuron.2014.12.032 · Cited by 2,102
An Essential Role for Senescent Cells in Optimal Wound Healing through Secretion of PDGF-AA
Demaria, M., Ohtani, N., Youssef, S. A., Rodier, F., Toussaint, W., Mitchell, J. R., Laberge, R.-M., Vijg, J., Van Steeg, H., Dollé, M. E. T., et al. (2014) · Developmental Cell · doi:10.1016/j.devcel.2014.11.012 · Cited by 2,045
Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints
Bartkova, J., Rezaei, N., Liontos, M., Karakaidos, P., Kletsas, D., Issaeva, N., Vassiliou, L.-V. F., Kolettas, E., Niforou, K., Zoumpourlis, V. C., et al. (2006) · Nature · doi:10.1038/nature05268 · Cited by 1,986
How neuroinflammation contributes to neurodegeneration
Ransohoff, R. M. (2016) · Science · doi:10.1126/science.aag2590 · Cited by 1,967 · cited 4×
“Interestingly, a common feature of PD patients and mouse models is the accumulation of activated microglia and astrocytes, which would promote increased local concentrations of inflammatory mediators and ROS (84).”
InfluentialOlovnikov (1973) · doi:10.1016/0022-5193(73)90198-7 · Cited by 1,847
Oncogene-induced senescence is a DNA damage response triggered by DNA hyper-replication
Di Micco, R., Fumagalli, M., Cicalese, A., Piccinin, S., Gasparini, P., Luise, C., Schurra, C., Garre’, M., Giovanni Nuciforo, P., Bensimon, A., et al. (2006) · Nature · doi:10.1038/nature05327 · Cited by 1,821
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
The ATM protein kinase: regulating the cellular response to genotoxic stress, and more
Shiloh, Y., & Ziv, Y. (2013) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3546 · Cited by 1,649
Cellular senescence mediates fibrotic pulmonary disease
Schafer, M. J., White, T. A., Iijima, K., Haak, A. J., Ligresti, G., Atkinson, E. J., Oberg, A. L., Birch, J., Salmonowicz, H., Zhu, Y., et al. (2017) · Nature Communications · doi:10.1038/ncomms14532 · Cited by 1,613 · cited 1×
“Using mouse models, elimination of these cells, through either genetic means or senolytic therapies, has largely shown beneficial impacts, irrespective of the disease or condition investigated (29–31, 99, 100).”
Astrocyte activation and reactive gliosis
Pekny, M., & Nilsson, M. (2005) · Glia · doi:10.1002/glia.20207 · Cited by 1,611
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 · cited 5×
“…potentially senolytic molecules and strategies, including piperlongumine (94), dasatinib (95), quercetin (95), the proprietary compound UBX0101 (31), a FOXO4 peptide that promotes p53-dependent apoptosis (96), and HSP90 inhibitors (97), have also been identified, demonstrating that there are…”
InfluentialSelf-citationInk4a/Arf expression is a biomarker of aging
Krishnamurthy, J., Torrice, C., Ramsey, M. R., Kovalev, G. I., Al-Regaiey, K., Su, L., & Sharpless, N. E. (2004) · Journal of Clinical Investigation · doi:10.1172/jci22475 · Cited by 1,486
Monetary Costs of Dementia in the United States
Hurd, M. D., Martorell, P., Delavande, A., Mullen, K. J., & Langa, K. M. (2013) · New England Journal of Medicine · doi:10.1056/nejmsa1204629 · Cited by 1,484
Baar, M. P., Brandt, R. M. C., Putavet, D. A., Klein, J. D. D., Derks, K. W. J., Bourgeois, B. R. M., Stryeck, S., Rijksen, Y., van Willigenburg, H., Feijtel, D. A., et al. (2017) · Cell · doi:10.1016/j.cell.2017.02.031 · Cited by 1,454
Senescent 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-citationSenescent intimal foam cells are deleterious at all stages of atherosclerosis
Childs, B. G., Baker, D. J., Wijshake, T., Conover, C. A., Campisi, J., & van Deursen, J. M. (2016) · Science · doi:10.1126/science.aaf6659 · Cited by 1,195
Self-citationForging a signature of in vivo senescence
Sharpless, N. E., & Sherr, C. J. (2015) · Nature Reviews Cancer · doi:10.1038/nrc3960 · Cited by 1,104
Lamin B1 loss is a senescence-associated biomarker
Freund, A., Laberge, R.-M., Demaria, M., & Campisi, J. (2012) · Molecular Biology of the Cell · doi:10.1091/mbc.e11-10-0884 · Cited by 1,046
Directed elimination of senescent cells by inhibition of BCL-W and BCL-XL
Yosef, R., Pilpel, N., Tokarsky-Amiel, R., Biran, A., Ovadya, Y., Cohen, S., Vadai, E., Dassa, L., Shahar, E., Condiotti, R., et al. (2016) · Nature Communications · doi:10.1038/ncomms11190 · Cited by 1,032
Increasing p16INK4a expression decreases forebrain progenitors and neurogenesis during ageing
Molofsky, A. V., Slutsky, S. G., Joseph, N. M., He, S., Pardal, R., Krishnamurthy, J., Sharpless, N. E., & Morrison, S. J. (2006) · Nature · doi:10.1038/nature05091 · Cited by 972 · cited 1×
“…impairing adult neurogenesis, genetic inactivation of p16 INK4A in mice results in an increased capacity for self-renewal of neuronal stem cells in the subventricular zone of the olfactory bulb of aged mice (62). ing additional features of senescence besides being permanently growth-arrested.”
Senescence-messaging secretome: SMS-ing cellular stress
Kuilman, T., & Peeper, D. S. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2560 · Cited by 909
A new murine model of accelerated senescence
Takeda, T., HOSOKAWA, M., TAKESHITA, S., Irino, M., Higuchi, K., Matsushita, T., Tomita, Y., Yasuhira, K., Hamamoto, H., & Shimizu, K. (1981) · Mechanisms of Ageing and Development · doi:10.1016/0047-6374(81)90084-1 · Cited by 871
Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis
Sharpless, N. E., Bardeesy, N., Lee, K.-H., Carrasco, D., Castrillon, D. H., Aguirre, A. J., Wu, E. A., Horner, J. W., & DePinho, R. A. (2001) · Nature · doi:10.1038/35092592 · Cited by 848
Dementia and Alzheimer Disease Incidence: A Prospective Cohort Study
Kukull, W. A., Higdon, R., Bowen, J. D., McCormick, W. C., Teri, L., Schellenberg, G. D., van Belle, G., Jolley, L., & Larson, E. B. (2002) · Archives of Neurology · doi:10.1001/archneur.59.11.1737 · Cited by 806
Senescing human cells and ageing mice accumulate DNA lesions with unrepairable double-strand breaks
Sedelnikova, O. A., Horikawa, I., Zimonjic, D. B., Popescu, N. C., Bonner, W. M., & Barrett, J. C. (2004) · Nature Cell Biology · doi:10.1038/ncb1095 · Cited by 790
Molecular mechanisms of neurodegeneration in Alzheimer's disease
Crews, L., & Masliah, E. (2010) · Human Molecular Genetics · doi:10.1093/hmg/ddq160 · Cited by 772 · cited 1×
“org Volume 128 Number 4 April 2018 and neuro fibrillary tangle aggregates of hyperphosphorylated or misfolded tau protein (77).”
Does neuroinflammation fan the flame in neurodegenerative diseases?
Frank-Cannon, T. C., Alto, L. T., McAlpine, F. E., & Tansey, M. G. (2009) · Molecular Neurodegeneration · doi:10.1186/1750-1326-4-47 · Cited by 751
Identification of HSP90 inhibitors as a novel class of senolytics
Fuhrmann-Stroissnigg, H., Ling, Y. Y., Zhao, J., McGowan, S. J., Zhu, Y., Brooks, R. W., Grassi, D., Gregg, S. Q., Stripay, J. L., Dorronsoro, A., et al. (2017) · Nature Communications · doi:10.1038/s41467-017-00314-z · Cited by 701
Microglia derived from aging mice exhibit an altered inflammatory profile
Sierra, A., Gottfried‐Blackmore, A. C., McEwen, B. S., & Bulloch, K. (2007) · Glia · doi:10.1002/glia.20468 · Cited by 688
Yankner, B. A., Lu, T., & Loerch, P. (2008) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev.pathmechdis.2.010506.092044 · Cited by 677
Opposing effects of Ets and Id proteins on p16INK4a expression during cellular senescence
Ohtani, N., Zebedee, Z., Huot, T. J. G., Stinson, J. A., Sugimoto, M., Ohashi, Y., Sharrocks, A. D., Peters, G., & Hara, E. (2001) · Nature · doi:10.1038/35059131 · Cited by 654
Mehta, D. G., Jackson, R., Paul, G., Shi, J., & Sabbagh, M. N. (2017) · Expert Opinion on Investigational Drugs · doi:10.1080/13543784.2017.1323868 · Cited by 626
Jurk, D., Wang, C., Miwa, S., Maddick, M., Korolchuk, V., Tsolou, A., Gonos, E. S., Thrasivoulou, C., Jill Saffrey, M., Cameron, K., et al. (2012) · Aging Cell · doi:10.1111/j.1474-9726.2012.00870.x · Cited by 598
Astrocyte Senescence as a Component of Alzheimer’s Disease
Bhat, R., Crowe, E. P., Bitto, A., Moh, M., Katsetos, C. D., Garcia, F. U., Johnson, F. B., Trojanowski, J. Q., Sell, C., & Torres, C. (2012) · PLoS ONE · doi:10.1371/journal.pone.0045069 · Cited by 586
Rodier, F., Muñoz, D. P., Teachenor, R., Chu, V., Le, O., Bhaumik, D., Coppé, J.-P., Campeau, E., Beauséjour, C. M., Kim, S.-H., et al. (2011) · Journal of Cell Science · doi:10.1242/jcs.071340 · Cited by 535
Coppé, J.-P., Patil, C. K., Rodier, F., Krtolica, A., Beauséjour, C. M., Parrinello, S., Hodgson, J. G., Chin, K., Desprez, P.-Y., & Campisi, J. (2010) · PLoS ONE · doi:10.1371/journal.pone.0009188 · Cited by 455
p53-dependent release of Alarmin HMGB1 is a central mediator of senescent phenotypes
Davalos, A. R., Kawahara, M., Malhotra, G. K., Schaum, N., Huang, J., Ved, U., Beausejour, C. M., Coppe, J.-P., Rodier, F., & Campisi, J. (2013) · Journal of Cell Biology · doi:10.1083/jcb.201206006 · Cited by 439
Abnormal expression of the cell cycle regulators P16 and CDK4 in Alzheimer's disease.
McShea, A., Harris, P. L. R., Webster, K. R., Wahl, A. F., & Smith, M. A. (1997) · Europe PMC (PubMed Central) · Cited by 422
Opposing roles for p16Ink4a and p19Arf in senescence and ageing caused by BubR1 insufficiency
Baker, D. J., Perez-Terzic, C., Jin, F., Pitel, K. S., Niederländer, N. J., Jeganathan, K., Yamada, S., Reyes, S., Rowe, L., Hiddinga, H. J., et al. (2008) · Nature Cell Biology · doi:10.1038/ncb1744 · Cited by 408 · cited 2×
“Subsequent studies using the INK-ATTAC model determined that senescent cells drive various natural age-related pathologies, shorten life, and promote the age-associated diseases atherosclerosis and osteoarthritis (20, 29–31).”
Self-citationAlimonti, A., Nardella, C., Chen, Z., Clohessy, J. G., Carracedo, A., Trotman, L. C., Cheng, K., Varmeh, S., Kozma, S. C., Thomas, G., et al. (2010) · Journal of Clinical Investigation · doi:10.1172/jci40535 · Cited by 374
Calabrese, V., Santoro, A., Monti, D., Crupi, R., Di Paola, R., Latteri, S., Cuzzocrea, S., Zappia, M., Giordano, J., Calabrese, E. J., et al. (2018) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2017.10.379 · Cited by 356
Cellular senescence and organismal aging
Jeyapalan, J. C., & Sedivy, J. M. (2008) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2008.04.001 · Cited by 351
Salminen, A., Ojala, J., Kaarniranta, K., Haapasalo, A., Hiltunen, M., & Soininen, H. (2011) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2011.07738.x · Cited by 333
Down syndrome: Cognitive phenotype
Silverman, W. (2007) · Mental Retardation and Developmental Disabilities Research Reviews · doi:10.1002/mrdd.20156 · Cited by 324
Coppé, J.-P., Patil, C. K., Rodier, F., Sun, Y., Muñoz, D. P., Goldstein, J., Nelson, P. S., Desprez, P.-Y., & Campisi, J. (2008) · PLoS Biology · doi:10.1371/journal.pbio.0060301 · Cited by 302 · cited 9×
“The expectation would then be that senolytic therapy reduces the SASP and markers of disease.”
InfluentialBachstetter, A. D., Xing, B., de Almeida, L., Dimayuga, E. R., Watterson, D. M., & Van Eldik, L. J. (2011) · Journal of Neuroinflammation · doi:10.1186/1742-2094-8-79 · Cited by 282
Discovery of piperlongumine as a potential novel lead for the development of senolytic agents
Wang, Y., Chang, J., Liu, X., Zhang, X., Zhang, S., Zhang, X., Zhou, D., & Zheng, G. (2016) · Aging · doi:10.18632/aging.101100 · Cited by 274
Evidence That Aging And Amyloid Promote Microglial Cell Senescence
Flanary, B. E., Sammons, N. W., Nguyen, C., Walker, D., & Streit, W. J. (2007) · Rejuvenation Research · doi:10.1089/rej.2006.9096 · Cited by 272
Exercise Prevents Diet-Induced Cellular Senescence in Adipose Tissue
Schafer, M. J., White, T. A., Evans, G., Tonne, J. M., Verzosa, G. C., Stout, M. B., Mazula, D. L., Palmer, A. K., Baker, D. J., Jensen, M. D., et al. (2016) · Diabetes · doi:10.2337/db15-0291 · Cited by 267
Self-citationVascular Cell Senescence Contributes to Blood–Brain Barrier Breakdown
Yamazaki, Y., Baker, D. J., Tachibana, M., Liu, C.-C., van Deursen, J. M., Brott, T. G., Bu, G., & Kanekiyo, T. (2016) · Stroke · doi:10.1161/strokeaha.115.010835 · Cited by 263
Self-citationCockayne syndrome: Clinical features, model systems and pathways
Karikkineth, A. C., Scheibye-Knudsen, M., Fivenson, E., Croteau, D. L., & Bohr, V. A. (2017) · Ageing Research Reviews · doi:10.1016/j.arr.2016.08.002 · Cited by 262
Expression of the cyclin-dependent kinase inhibitor p16 in Alzheimerʼs disease
Lars Rödel, T. A., Gärtner, U., & Holzer, M. (1996) · NeuroReport · doi:10.1097/00001756-199611250-00050 · Cited by 250
Cell Senescence: Role in Aging and Age-Related Diseases
Campisi, J., & Robert, L. (2014) · Interdisciplinary Topics in Gerontology and Geriatrics · doi:10.1159/000358899 · Cited by 240
Meta-analysis of Telomere Length in Alzheimer’s Disease
Forero, D. A., González-Giraldo, Y., López-Quintero, C., Castro-Vega, L. J., Barreto, G. E., & Perry, G. (2016) · The Journals of Gerontology Series A: Biological Sciences and Medical Sciences · doi:10.1093/gerona/glw053 · Cited by 229
β-Amyloid precursor polypeptide in SAMP8 mice affects learning and memory
Morley, J. E., Kumar, V. B., Bernardo, A. E., Farr, S. A., Uezu, K., Tumosa, N., & Flood, J. F. (2000) · Peptides · doi:10.1016/s0196-9781(00)00342-9 · Cited by 222
The senescence accelerated mouse (SAMP8) as a model for oxidative stress and Alzheimer's disease
Morley, J. E., Armbrecht, H. J., Farr, S. A., & Kumar, V. B. (2011) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2011.11.015 · Cited by 205
Stress-induced senescence in human and rodent astrocytes
Bitto, A., Sell, C., Crowe, E., Lorenzini, A., Malaguti, M., Hrelia, S., & Torres, C. (2010) · Experimental Cell Research · doi:10.1016/j.yexcr.2010.06.021 · Cited by 204
Nissan, X., Blondel, S., Navarro, C. L., Maury, Y., Denis, C., Girard, M., Martinat, C., Sandre‐Giovannoli, A. D., Lévy, N., & Peschanski, M. (2012) · Cell Reports · doi:10.1016/j.celrep.2012.05.015 · Cited by 183
Evidence of DNA damage in Alzheimer disease: phosphorylation of histone H2AX in astrocytes
Myung, N.-H., Zhu, X., Kruman, I. I., Castellani, R. J., Petersen, R. B., Siedlak, S. L., Perry, G., Smith, M. A., & Lee, H.-G. (2008) · AGE · doi:10.1007/s11357-008-9050-7 · Cited by 170
Self-citationGlial influences on BBB functions and molecular players in immune cell trafficking
Lécuyer, M., Kébir, H., & Prat, A. (2015) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2015.10.004 · Cited by 166
Neuronal expression of cycline dependent kinase inhibitors of the INK4 family in Alzheimer's disease
Arendt, T., Holzer, M., & Gärtner, U. (1998) · Journal of Neural Transmission · doi:10.1007/s007020050104 · Cited by 137
Wong, E. S. M., Guezennec, X. L., Demidov, O. N., Marshall, N. T., Wang, S. T., Krishnamurthy, J., Sharpless, N. E., Dunn, N. R., & Bulavin, D. V. (2009) · Developmental Cell · doi:10.1016/j.devcel.2009.05.009 · Cited by 131
Weirich, H. G., Weirich, H. G., Gruber, B., Schweiger, M. R., & Hirsch‐Kauffmann, M. (1994) · Mutation Research/DNAging · doi:10.1016/0921-8734(94)90006-x · Cited by 113
Changes in the Transcriptome of Human Astrocytes Accompanying Oxidative Stress-Induced Senescence
Crowe, E. P., Tuzer, F., Gregory, B. D., Donahue, G., Gosai, S. J., Cohen, J., Leung, Y. Y., Yetkin, E., Nativio, R., Wang, L.-S., et al. (2016) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2016.00208 · Cited by 110
Newington, J. T., Harris, R. A., & Cumming, R. C. (2013) · Journal of Neurodegenerative Diseases · doi:10.1155/2013/234572 · Cited by 109
Emerging roles of microglial activation and non-motor symptoms in Parkinson's disease
Doorn, K. J., Lucassen, P. J., Boddeke, H. W. G. M., Prins, M., Berendse, H. W., Drukarch, B., & van Dam, A. (2012) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2012.06.005 · Cited by 98
Fate of microglia during HIV‐1 infection: From activation to senescence?
Chen, N. C., Partridge, A. T., Sell, C., Torres, C. A., & Martín‐García, J. (2016) · Glia · doi:10.1002/glia.23081 · Cited by 94
Mitochondrial DNA damage induces apoptosis in senescent cells
Laberge, R.-M., Adler, D., DeMaria, M., Mechtouf, N., Teachenor, R., Cardin, G. B., Desprez, P.-Y., Campisi, J., & Rodier, F. (2013) · Cell Death & Disease · doi:10.1038/cddis.2013.199 · Cited by 82
Romanov, V. S., Igotti, M. V., Svetlikova, S. B., Bykova, T. V., Zubova, S. G., Aksenov, N. D., Fornace, A. J., Pospelova, T. V., & Pospelov, V. A. (2010) · Cell Cycle · doi:10.4161/cc.9.19.13160 · Cited by 81
The Mdm network and its regulation of p53 activities: a rheostat of cancer risk
Eischen, C. M., & Lozano, G. (2014) · Human Mutation · doi:10.1002/humu.22524 · Cited by 79
Repeated Lipopolysaccharide Stimulation Induces Cellular Senescence in BV2 Cells
Yu, H.-M., Zhao, Y.-M., Luo, X.-G., Feng, Y., Ren, Y., Shang, H., He, Z.-Y., Luo, X.-M., Chen, S.-D., & Wang, X.-Y. (2012) · Neuroimmunomodulation · doi:10.1159/000330254 · Cited by 76
Telomere length in Parkinson's disease: A meta-analysis
Forero, D. A., González-Giraldo, Y., López-Quintero, C., Castro-Vega, L. J., Barreto, G. E., & Perry, G. (2016) · Experimental Gerontology · doi:10.1016/j.exger.2016.01.002 · Cited by 70
Tavana, O., Benjamin, C. L., Puebla‐Osorio, N., Sang, M., Ullrich, S. E., Ananthaswamy, H. N., & Zhu, C. (2010) · Cell Cycle · doi:10.4161/cc.9.16.12688 · Cited by 62
Astrocyte senescence and metabolic changes in response to HIV antiretroviral therapy drugs
Cohen, J., D’Agostino, L., Wilson, J., Tuzer, F., & Torres, C. (2017) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2017.00281 · Cited by 58
Yu, C., Narasipura, S. D., Richards, M. H., Hu, X., Yamamoto, B., & Al‐Harthi, L. (2017) · Aging Cell · doi:10.1111/acel.12593 · Cited by 57
Mutant mice with small amounts of BubR1 display accelerated age-related gliosis
Hartman, T. K., Wengenack, T. M., Poduslo, J. F., & van Deursen, J. M. (2007) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2006.05.012 · Cited by 54
Stress-induced microglial activation may facilitate the progression of neurodegenerative disorders
Sugama, S. (2009) · Medical Hypotheses · doi:10.1016/j.mehy.2009.02.047 · Cited by 52
Herbig, U., Wei, W., Dutriaux, A., Jobling, W. A., & Sedivy, J. M. (2003) · Aging Cell · doi:10.1046/j.1474-9728.2003.00067.x · Cited by 51
Cognitive Phenotype in Ataxia-Telangiectasia
Hoche, F., Frankenberg, E., Rambow, J., Theis, M., Harding, J. A., Qirshi, M., Seidel, K., Barbosa‐Sicard, E., Porto, L., Schmahmann, J. D., et al. (2014) · Pediatric Neurology · doi:10.1016/j.pediatrneurol.2014.04.027 · Cited by 50
Responses of human embryonic stem cells and their differentiated progeny to ionizing radiation
Zou, Y., Zhang, N., Ellerby, L. M., Davalos, A. R., Zeng, X., Campisi, J., & Desprez, P.-Y. (2012) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2012.08.043 · Cited by 41
Age-related decline in BubR1 impairs adult hippocampal neurogenesis
Yang, Z., Jun, H., Choi, C.-I., Yoo, K. H., Cho, C. H., Hussaini, S. M. Q., Simmons, A. J., Kim, S., van Deursen, J. M., Baker, D. J., et al. (2017) · Aging Cell · doi:10.1111/acel.12594 · Cited by 40
Self-citationThe progeroid gene BubR1 regulates axon myelination and motor function
Choi, C.-I., Yoo, K. H., Hussaini, S. M. Q., Jeon, B. T., Welby, J., Gan, H., Scarisbrick, I. A., Zhang, Z., Baker, D. J., van Deursen, J. M., et al. (2016) · Aging · doi:10.18632/aging.101032 · Cited by 26
Self-citation
Flagged first, then by citations
1 of the 102 references couldn’t be matched to a known paper.
Cited by
Sorted by citations
Ageing as a risk factor for neurodegenerative disease
Hou, Y., Dan, X., Babbar, M., Wei, Y., Hasselbalch, S. G., Croteau, D. L., & Bohr, V. A. (2019) · Nature Reviews Neurology · doi:10.1038/s41582-019-0244-7 · Cited by 3,310
Aging and aging-related diseases: from molecular mechanisms to interventions and treatments
Guo, J., Huang, X., Dou, L., Yan, M., Shen, T., Tang, W., & Li, J. (2022) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-01251-0 · Cited by 1,976
Zhang, P., Kishimoto, Y., Grammatikakis, I., Gottimukkala, K., Cutler, R. G., Zhang, S., Abdelmohsen, K., Bohr, V. A., Misra Sen, J., Gorospe, M., et al. (2019) · Nature Neuroscience · doi:10.1038/s41593-019-0372-9 · Cited by 977
Measuring biological aging in humans: a quest
Ferrucci, L., Gonzalez‐Freire, M., Fabbri, E., Simonsick, E., Tanaka, T., Moore, Z., Salimi, S., Sierra, F., & de Cabo, R. (2020) · Aging Cell · doi:10.1111/acel.13080 · Cited by 781
Role of p53 in the Regulation of Cellular Senescence
Mijit, M., Caracciolo, V., Melillo, A., Amicarelli, F., & Giordano, A. (2020) · Biomolecules · doi:10.3390/biom10030420 · Cited by 639
Metadata
- Authors
- Baker, D. J., & Petersen, R. C.
- Affiliations
- Mayo Clinic (US)
- Venue
- Journal of Clinical Investigation
- Published
- 2018-02-19
- Volume
- 128
- Issue
- 4
- Pages
- 1208-1216
- ISSN
- 0021-9738 (ISSN-L)
- 1558-8238
- PMC
- PMC5873891
- OpenAlex
- W2789191208
- Semantic Scholar
- 2532232dad192413fd93fdbee252c09f546c10ac
- Cited by
- 514
- References
- 102
- Citations by year
- 2026: 57 · 2025: 88 · 2024: 76 · 2023: 58 · 2022: 69 · 2021: 66 · 2020: 58 · 2019: 31 · 2018: 11
- FWCI
- 5.46
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ellison Medical Foundation
- Mayo Clinic (55905)
- Glenn Foundation for Medical Research
- Fondation pour la Recherche Médicale
- National Institutes of Health
- National Institute on Aging (U01AG006786, R01AG053229, P50AG016574)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- cellular senescence, brain aging, neurodegenerative diseases, Parkinson's disease, Alzheimer's disease, senescence-associated secretory phenotype, age-related cognitive impairment, senolytics, senolytic therapy, cell cycle arrest
- MeSH terms
- Aging, Alzheimer Disease, Brain, Chronic Disease, Humans, Cellular Senescence, Cell Cycle Checkpoints, 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.
A language model drew the claims from the paper on 2026-10-05, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-05 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
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
