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.
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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)
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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In 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
plaindirect- Asserted: passes — The authors put it forward as true.
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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
“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
plain- Asserted: passes — The authors put it forward as true.
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In 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
plaindirect- Asserted: passes — The authors put it forward as true.
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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
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In 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
plaincorrelational- Asserted: passes — The authors put it forward as true.
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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
“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
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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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
plaindirect- Asserted: passes — The authors put it forward as true.
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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
“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
plain- Asserted: passes — The authors put it forward as true.
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In 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
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- 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)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It 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
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It 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
plaindirect- Asserted: passes — The authors put it forward as true.
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It 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.
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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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
“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.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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It 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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“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
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
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It 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
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
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The limited in vitro lifetime of human diploid cell strains
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Abbott, N. J., Rönnbäck, L., & Hansson, E. (2006) · Nature Reviews Neuroscience · doi:10.1038/nrn1824 · Cited by 5,595
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Blood CDKN2A Gene Expression in Aging and Neurodegenerative Diseases
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Loss-of-function of p53 isoform Δ113p53 accelerates brain aging in zebrafish
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Endothelial CYP2J2 overexpression restores the BRB via METTL3 ‐mediated ANXA1 upregulation
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Cellular senescence: A novel therapeutic target for central nervous system diseases
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Interaction of Cannabis Use and Aging: From Molecule to Mind
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Multifaceted roles of Meg3 in cellular senescence and atherosclerosis
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Tau proteins and senescent Cells: Targeting aging pathways in Alzheimer’s disease
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Senolytic therapies for cardiovascular aging: tackling fibrosis and metabolic dysfunction
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Senescence in RASopathies, a possible novel contributor to a complex pathophenoype
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Recent Advances in Strategies for Imaging Detection and Intervention of Cellular Senescence
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Accelerated Cellular Senescence in Progressive Multiple Sclerosis: A Histopathological Study
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Human Monocytes Plasticity in Neurodegeneration
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Somatic mosaicism in the diseased brain
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Therapeutic Potential of PTB Inhibition Through Converting Glial Cells to Neurons in the Brain
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Effects of Redox Homeostasis and Mitochondrial Damage on Alzheimer’s Disease
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Vascular rejuvenation is geroprotective
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Cellular Senescence in Glial Cells: Implications for Multiple Sclerosis
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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 ›
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