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)
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
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“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
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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
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
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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
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
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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
“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
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Items 301–400 of 518
IFN-γ Triggered IFITM2 Expression to Induce Malignant Phenotype in Elderly GBM
Liang, T., Wang, X., Wang, Y., & Ma, W. (2023) · Journal of Molecular Neuroscience · doi:10.1007/s12031-023-02156-5 · Cited by 7
Giant cell arteritis: update on pathogenesis and clinical implications
Ibrahim, H., & Bari, C. D. (2024) · Current Opinion in Rheumatology · doi:10.1097/bor.0000000000001051 · Cited by 7
The Biological Intersection Between Chemotherapy-Related Cognitive Impairment and Alzheimer Disease
Torre, M., Zanella, C. A., & Feany, M. Β. (2025) · American Journal Of Pathology · doi:10.1016/j.ajpath.2024.12.013 · Cited by 8
Komleva, Y. K., Shpiliukova, K. A., Bondar, N., Salmina, A. B., Хилажева, Е. Д., Illarioshkin, S. N., & Пирадов, М. А. (2025) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2025.1562453 · Cited by 9
The original colorimetric method to detect cellular senescence
Dimri, M., & Dimri, G. P. (2022) · Methods in cell biology · doi:10.1016/bs.mcb.2022.09.005 · Cited by 7
Kostyunina, O. V., Komoltsev, I. G., Timokhova, A. V., Belikova, A., Balan, S. I., & Gulyaeva, N. V. (2024) · Neurochemical Journal · doi:10.1134/s1819712424700557 · Cited by 8
Elimination of senescent cells prevents neurodegeneration in mice
Penney, J., & Tsai, L. (2018) · Nature · doi:10.1038/d41586-018-06677-7 · Cited by 7
Casoli, T., Giuli, C., Balietti, M., Fabbietti, P., & Conti, F. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21145110 · Cited by 6
Wang, G., Wang, X., Zheng, X., Sun, S., Zhao, J., Ying, L., & Mao, Y. (2022) · Neuroscience Research · doi:10.1016/j.neures.2022.08.005 · Cited by 7
Getting Too Old Too Quickly for Their Job: Senescent Glial Cells Promote Neurodegeneration
Gosselin, D., & Rivest, S. (2018) · Neuron · doi:10.1016/j.neuron.2018.11.006 · Cited by 7
Wang, S., Li, B., Cai, Z., Hugo, C., Li, J., Sun, Y. E., Lü, Q., Remaley, A. T., Julia, T. C. W., Chui, H. C., et al. (2024) · Research Square · doi:10.21203/rs.3.rs-4373201/v1 · Cited by 7
Chen, Q., Zhou, T., Zhang, C., & Zhong, X. (2024) · Heliyon · doi:10.1016/j.heliyon.2024.e27069 · Cited by 6
Astragaloside IV confronts amyloid-beta-induced astrocyte senescence via hsp90aa1
Xia, Y., Zeng, R., & Cao, Y. (2024) · Journal of Applied Biomedicine · doi:10.32725/jab.2024.015 · Cited by 6
Bursts of brain erosion: seizures and age-dependent neurological vulnerability
Cresto, N., Givalois, L., Badaut, J., Janvier, A., Génin, A., Audinat, É., Brewster, A. L., & Marchi, N. (2024) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2024.11.003 · Cited by 6
Pacca-Corrêa, J. B. L., Fernandes, B. M., Siqueira, M., Schafbenker, R., Baumart, G. J., Damico, I. V., Gomes, F. C. A., & Matias, I. C. P. (2026) · Neurochemical Research · doi:10.1007/s11064-026-04709-7 · Cited by 6
Costa, D. G., Gee, L., Lee, G., Gomez, L. S., Franco, A. C., Vizioli, M. G., Valdivieso, K., Zhang, L. J., Pirius, N., Martini, H., et al. (2026) · EMBO Molecular Medicine · doi:10.1038/s44321-026-00400-0 · Cited by 7
Integrated Multimodal Omics and Dietary Approaches for the Management of Neurodegeneration
Murai, T., & Matsuda, S. (2023) · Epigenomes · doi:10.3390/epigenomes7030020 · Cited by 5
Senolytics prevent age-associated changes in female mice brain
Faria, O. W., Soares, M. S. P., de Mello, J. E., Alvez, F. L., Luduvico, K. P., Garcia, D. N., Schneider, A., Masternak, M. M., Spanevello, R. M., & Stefanello, F. M. (2024) · Neuroscience Letters · doi:10.1016/j.neulet.2024.137730 · Cited by 6
Xu, Y., Liu, S., Zhou, Z., Qin, H., Zhang, Y., Zhang, G., Ma, H., Han, X., Liu, H., & Liu, Z. (2024) · Human Molecular Genetics · doi:10.1093/hmg/ddae189 · Cited by 6
Lee, Y., Lee, J., Kim, J., Cho, S. A., Lee, H.-J., Geum, D., Park, D., & Kim, J. (2025) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2025.01.050 · Cited by 6
Telomerase inhibition decreases esophageal squamous carcinoma cell migration and invasion
Li, J., Dong, G., Song, J., Tan, G., & Wu, X. (2020) · Oncology Letters · doi:10.3892/ol.2020.11810 · Cited by 6
Cholinergic Senescence in the Ts65Dn Mouse Model for Down Syndrome
Kirstein, M., Cambrils, A., Segarra, A., Melero, A., & Varea, E. (2022) · Neurochemical Research · doi:10.1007/s11064-022-03659-0 · Cited by 9
Targeting the microbiota-mitochondria crosstalk in neurodegeneration with senotherapeutics
Homolak, J. (2023) · Advances in protein chemistry and structural biology · doi:10.1016/bs.apcsb.2023.02.018 · Cited by 8
Dotou, M., L’honoré, A., Moumné, R., & Amri, C. E. (2024) · Journal of Natural Products · doi:10.1021/acs.jnatprod.3c01195 · Cited by 8
Chen, M., Liu, M., Chen, J., Liu, X., Tang, L., Wang, C., Yu, Z., Zhang, Y., & Tian, J. (2024) · Molecular Nutrition & Food Research · doi:10.1002/mnfr.202300469 · Cited by 6
DNA Methylation in Neuronal Development and Disease
Bruggeman, E. C., & Yao, B. (2019) · RNA technologies · doi:10.1007/978-3-030-14792-1_5 · Cited by 7
Single-cell RNA-Sequencing in Neuroscience
Mayer, S., Khakipoor, S., Droemer, M. A., & Cozetto, D. A. (2019) · e-Neuroforum · doi:10.1515/nf-2019-0021 · Cited by 6
Inhibition of miR-21 Promotes Cellular Senescence in NT2-Derived Astrocytes
Balint, V., Ninković, D. S., Anastasov, N., Lazić, S., Kovačević‐Grujičić, N., Stevanović, M. J., & Lazic, A. (2021) · Biochemistry (Moscow) · doi:10.1134/s0006297921110079 · Cited by 8
A Comprehensive Update of Cerebral Organoids between Applications and Challenges
Li, X., Shopit, A., & Wang, J. (2022) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2022/7264649 · Cited by 6
Enomoto, S., Hur, Y. H., Solodova, T., Neumann, J., Cerione, R. A., & Antonyak, M. A. (2025) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2025.110821 · Cited by 5
Aggregation and Propagation of α‐Synuclein in Parkinson's Disease: A Bibliometric Perspective
Zhang, X., Ma, Y., Gao, G., & Wu, Q. (2025) · Brain and Behavior · doi:10.1002/brb3.71023 · Cited by 5
Evaluating senescence-targeted approaches in Alzheimer’s Disease: What we know and what lies ahead
Doshi, P. P., Desale, S. H., Khutale, A. A., Sabarathinam, S., & Suresh, S. (2026) · Ageing Research Reviews · doi:10.1016/j.arr.2026.103029 · Cited by 7
Lemus, A. J. J., Tewelde, E., Bhala, R., Guan, A., Xu, A., & Benayoun, B. A. (2026) · Open Biology · doi:10.1098/rsob.250093 · Cited by 7
Cantero‐Fortiz, Y., Butler, C., Montalbán, X., & Boada, M. (2026) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2026.1805691 · Cited by 6
Sustaining Brain Youth by Neural Stem Cells: Physiological and Therapeutic Perspectives
dos Santos, M. A., Moreira, J. A. F., Santos, S. S., & Solá, S. (2025) · Molecular Neurobiology · doi:10.1007/s12035-025-04774-z · Cited by 7
Obesity‐related early structural alterations in the retina detected by optical coherence tomography
İnam, M. G., İnam, O., Gucer, D., Park, J., Amellal, Y., Tezel, T. H., & Tezel, G. (2025) · Diabetes Obesity and Metabolism · doi:10.1111/dom.16344 · Cited by 5
Effects of caloric restriction on retinal aging and neurodegeneration
Adornetto, A., Morrone, L. A., Satriano, A., Laganà, M. L., Licastro, E., Nucci, C., Corasaniti, M. T., Tonin, P., Bagetta, G., & Russo, R. (2020) · Progress in brain research · doi:10.1016/bs.pbr.2020.07.005 · Cited by 6
The role of Aβ in Alzheimer's Disease as an Evolutionary Outcome of Optimized Innate Immune Defense
Tatar, M. (2022) · The Journal of Prevention of Alzheimer s Disease · doi:10.14283/jpad.2022.68 · Cited by 6
Liu, M., Ma, N., Yang, X. J., Sun, M., Li, X., Liu, Y.-H., Chang, Q., & Hei, C. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-240001 · Cited by 5
SATB1, senescence and senescence‐related diseases
Qi, W., Bai, J., Wang, R., Zeng, X., & Zhang, L. (2024) · Journal of Cellular Physiology · doi:10.1002/jcp.31327 · Cited by 6
Wang, Y., Yang, M., Tu, Q., Tao, L., Liu, G., An, H. J., Zhang, H., Jin, J., Fan, J., Du, Y.-F., et al. (2020) · Circulation Journal · doi:10.1253/circj.cj-20-0210 · Cited by 5
Lam, V., Stephenson, A., Nesbit, M., Mamsa, S. S. A., Hackett, M. J., Takechi, R., & Mamo, J. C. L. (2019) · Nutritional Neuroscience · doi:10.1080/1028415x.2019.1664533 · Cited by 5
Saha, D., Kumar, S., Gupta, R. K., Kaur, I., Majumdar, S., Karunarathne, A., & Giri, L. (2025) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.5c00588 · Cited by 4
The Role of Oligodendrocytes in Alzheimer’s Disease Pathogenesis and Therapy
Guo, S., Yu, X., & Zhang, H. (2025) · Neuroglia · doi:10.3390/neuroglia6040046 · Cited by 5
Barron, A. E., Lin, J. S., Ryder, M. I., & Bergman, P. N. (2025) · Journal of Internal Medicine · doi:10.1111/joim.70060 · Cited by 4
Optical manipulation-based cell modulation and bio-microrobot
Pan, T., Bi, A., Li, B., & Xin, H. (2026) · Journal of Innovative Optical Health Sciences · doi:10.1142/s1793545826300120 · Cited by 4
Sweeney, E. M., Abate, G., Bakker, B. R. V., Mastinu, A., Lai, Y., Uberti, D. L., Nilsson, P., & Tambaro, S. (2026) · Aging Cell · doi:10.1111/acel.70478 · Cited by 5
Kushwaha, V., & Sahu, K. K. (2024) · Current Pharmaceutical Biotechnology · doi:10.2174/0113892010331845240802073645 · Cited by 5
Blockade of ZMIZ1‐GATA4 Axis Regulation Restores Youthfulness to Aged Cartilage
Nam, J., Woo, H., Yang, J.-H., Kim, S. J., Lee, K. P., Yu, J. H., Park, T. J., Eyun, S., & Yang, S. (2025) · Advanced Science · doi:10.1002/advs.202404311 · Cited by 4
Kasperová, B. J., Cinkajzlová, A., Horváth, L., Svoboda, P., Haluzı́k, M., & Hubáčková, S. (2025) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2025.1622107 · Cited by 4
Antisenescence therapies for age‐related bone loss: Target factors, medicines, biomedical materials
Zhu, Q., Hu, M., Wu, L., Wei, E., Pan, X., Liu, H., & Liu, Y. (2025) · Clinical and Translational Medicine · doi:10.1002/ctm2.70350 · Cited by 4
Khan, T., McFall, D. J., Hussain, A. I., Frayser, L. A., Casilli, T. P., Steck, M. C., Sánchez-Brualla, I., Kuehn, N. M., Cho, M., Barnes, J. A., et al. (2025) · Annals of Neurology · doi:10.1002/ana.78118 · Cited by 5
Future of Alzheimer's Disease Treatment: Combination Therapy and Precision Medicine
Fillit, H. M., Nisenbaum, L. K., & Burstein, A. H. (2023) · The Journal of Prevention of Alzheimer s Disease · doi:10.14283/jpad.2023.112 · Cited by 4
Sun, W., Sheng, X., Li, P., Li, R., Guo, Z., Hao, L., & Gong, Y. (2024) · Archiv der Pharmazie · doi:10.1002/ardp.202400263 · Cited by 4
Darvesh, S., Cash, M. K., Forrestall, K. L., Maillet, H., & Sands, D. C. (2025) · Aging · doi:10.18632/aging.206227 · Cited by 4
Screening Method for Identifying Toxicants Capable of Inducing Astrocyte Senescence
Woods, G., & Andersen, J. K. (2018) · Toxicological Sciences · doi:10.1093/toxsci/kfy181 · Cited by 4
Olinger, B., Banarjee, R., Dey, A. K., Tsitsipatis, D., Tanaka, T., Ram, A., Nyunt, T., Daya, G. N., Peng, Z., Cui, L., et al. (2024) · medRxiv · doi:10.1101/2024.08.01.24311368 · Cited by 4
Guo, X., Gao, F., Pan, B., Gao, F., Zhang, J., Wang, S., & Niu, Q. (2024) · Archives of Medical Science · doi:10.5114/aoms/192049 · Cited by 3
Maimaitiyiming, M., Yang, Y., Jia, X., & Zhang, X. (2025) · Age and Ageing · doi:10.1093/ageing/afaf132 · Cited by 4
Li, N., Huang, X., Zou, T., Wu, X., Yang, S., Xu, Z., Dai, J., Wang, K., & Zhao, J. (2025) · Oral Science and Homeostatic Medicine · doi:10.26599/oshm.2025.9610011 · Cited by 3
Castelli, V., Cesare, P., Bej, E., d’Angelo, M., & Volpe, A. R. (2025) · PLoS ONE · doi:10.1371/journal.pone.0320572 · Cited by 4
Potential connections between senescence and chemobrain: An early overview of literature
Melhem, N. Y., Qutifan, S., Alsalem, M., & Saleh, T. (2025) · Ageing Research Reviews · doi:10.1016/j.arr.2025.102896 · Cited by 4
Organelle Dysfunction and TNT-Mediated Aggregate Spreading in Neurodegeneration
Thomas, V., & Zurzolo, C. (2026) · Physiology · doi:10.1152/physiol.00048.2025 · Cited by 3
Rejili, M., Al‐kuraishy, H. M., Shokr, M. M., & Batiha, G. E. (2026) · Biogerontology · doi:10.1007/s10522-026-10457-6 · Cited by 3
Cellular senescence and nanoparticle-based therapies: Current developments and perspectives
Henschke, A., Mielcarek, A., Grześkowiak, B. F., Perrigue, P. M., Jaskot, K., Coy, E. L., & Moya, S. E. (2024) · Nanotechnology Reviews · doi:10.1515/ntrev-2023-0211 · Cited by 6
Michalettos, G., Clausen, F., Rostami, E., & Marklund, N. (2024) · Neurotherapeutics · doi:10.1016/j.neurot.2024.e00472 · Cited by 3
Datta, D. (2023) · The Journals of Gerontology Series A · doi:10.1093/gerona/glad134 · Cited by 3
Leung, E., Taskina, D., Schwab, N., & Hazrati, L. (2023) · Frontiers in Neuroscience · doi:10.3389/fnins.2023.1225226 · Cited by 3
Tsai, Y., González, E. A., Grodzki, A. C., Bruun, D. A., Saito, N. H., Harvey, D. J., & Lein, P. J. (2024) · Frontiers in Toxicology · doi:10.3389/ftox.2024.1360359 · Cited by 4
Cranial radiotherapy profoundly affects glia without inducing widespread cellular senescence
Kuil, L. E., van Scheppingen, R. H., Leter, Y. M., Röring, B. H., de Gooijer, M. C., Heijningen, C. L. V., Preković, S., Compter, A., van Tellingen, O., & Schagen, S. B. (2025) · Neuro-Oncology · doi:10.1093/neuonc/noaf146 · Cited by 3
The perception of family caregivers regarding the changes that occur after the diagnosis of dementia
Cesário, L. M. S., & Chariglione, I. P. F. S. (2018) · Revista Brasileira de Geriatria e Gerontologia · doi:10.1590/1981-22562018021.180123 · Cited by 3
de Oliveira, J. S., Sobral, A. D. V., Silva, T. V. D. A., Coriolano, M. D. G. W. D. S., & Lins, C. C. D. S. A. (2021) · Revista CEFAC · doi:10.1590/1982-0216/202123211220 · Cited by 3
Lio, R. M. S., Maugeri, A., Rosa, M. C. L., Giunta, G., Panella, M. M., Cianci, A., Caruso, M. A. T., Agodi, A., & Barchitta, M. (2022) · Scientific Reports · doi:10.1038/s41598-022-15370-9 · Cited by 3
Anggraini, D. R., Ilyas, S., Hasibuan, P. A. Z., Machrina, Y., Purba, A., Munir, D., Putra, I. B., & Betty, B. (2022) · Acta Informatica Medica · doi:10.5455/aim.2022.30.283-286 · Cited by 3
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Sloan, N. X., Mares, J., Daly, A. C., Grier, S., Haq, I., Jackson, C. A., Barretto, N., Casel, O., Kang, K., Khiste, S., et al. (2026) · Cell Genomics · doi:10.1016/j.xgen.2025.101127 · Cited by 2
Depletion of senescent cells improves surgery-induced neuroinflammation in aged mice
Perikamana, S. M., Newman, H., Shih, Y.-R. V., Duncan, L., Rather, H. A., Li, J., Velagapudi, R., Terrando, N., & Varghese, S. (2025) · PNAS Nexus · doi:10.1093/pnasnexus/pgaf103 · Cited by 3
Gong, X., Lu, W., Xiao, Q., Wang, X., Cui, C., & Tang, H. (2025) · Frontiers in Neurology · doi:10.3389/fneur.2025.1555586 · Cited by 2
Lambert, M., Miquel, G., Cagnone, G., Mury, P., Villeneuve, L. R., Lesage, F., Thorin‐Trescases, N., & Thorin, É. (2025) · GeroScience · doi:10.1007/s11357-025-01763-x · Cited by 2
New frontier for epilepsy treatment through targeting cellular senescence
Bello, S. T., Rafe, M. R., & Huang, F. (2025) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2025.111506 · Cited by 3
Gulej, R., Patai, R., Kiss, T., Chandragiri, S. S., Ekambaram, S., Nagaraja, R. Y., Nagy, D., Kordestan, K. V., Lakat, T., Tarantini, S., et al. (2025) · GeroScience · doi:10.1007/s11357-025-01953-7 · Cited by 4
Luo, G., Yu, J., Li, H., Fan, Q., Qian, Y., Zheng, L., Lin, J., Wu, G., Wu, Z., Zhao, J., et al. (2025) · Glia · doi:10.1002/glia.70116 · Cited by 2
Multiomic Analysis Reveals Molecular Pathways Associated with Intestinal Aggregation of α-Synuclein
Balsamo, J. M., Yan, Y., Thai, D., Cologna, S. M., & Bess, E. N. (2026) · ACS Chemical Biology · doi:10.1021/acschembio.5c00686 · Cited by 3
Neuroinflammation as a driver of Down syndrome-associated Alzheimer’s disease
Qu, H., Snorradóttir, Á. Ó., Gutierrez-Uzquiza, A., Kao, C., March, M., & Hakonarson, H. H. (2026) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2026.106513 · Cited by 2
Huang, H., Shi, H., Sun, J., Song, X., Yu, Y., Yan, L., Shi, F., Wang, W., & Zhang, Y. (2026) · Neuroscience Letters · doi:10.1016/j.neulet.2026.138597 · Cited by 2
Yılmaz, A., Park, H.-J., Ahn, E., & Bae, J. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27093930 · Cited by 4
Manni, E., Al‐kuraishy, H. M., Shokr, M. M., & Batiha, G. E. (2026) · Metabolic Brain Disease · doi:10.1007/s11011-026-01874-0 · Cited by 4
Neuroinflammatory and Neurodegenerative Roles of HIV-1 Tat: A Review of Recent Evidence
Williams, M. E., Muvenda, T., Mugwena, V., & Zulu, S. S. (2026) · Advances in experimental medicine and biology · doi:10.1007/978-3-032-24254-9_7 · Cited by 2
Salas-Venegas, V., López‐Díazguerrero, N. E., Carreto, R. J. R., Königsberg, M., & Chavarría, A. (2026) · Frontiers in Nutrition · doi:10.3389/fnut.2026.1824908 · Cited by 2
Payea, M. J., Gorospe, M., & Basisty, N. (2022) · Journal of Visualized Experiments · doi:10.3791/63835 · Cited by 2
Cellular Senescence in Physiological and Pathological Processes
Finicelli, M., Peluso, G., & Squillaro, T. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232113342 · Cited by 3
Glucose, glycolysis, and neurodegenerative disorders
Coelho, P., & Rego, A. C. (2023) · Elsevier eBooks · doi:10.1016/b978-0-323-91704-9.00012-4 · Cited by 2
Endothelial cellular senescence and tau accumulation: An interplay full of opportunities?
Oliveri, D., Moschetti, G., Griego, A., & Scarpa, E. (2024) · Ibrain · doi:10.1002/ibra.12154 · Cited by 2
Karliner, J. S., Liu, Y., & Merry, D. E. (2024) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2321408121 · Cited by 2
Phospholipid biogenesis maintains neuronal integrity during aging and axon regeneration
Park, S., Jin, Y., & Chisholm, A. D. (2025) · Genetics · doi:10.1093/genetics/iyaf122 · Cited by 2
Hu, N., Wang, K., Ge, X., Zhang, X., Zheng, X., & Sun, S. (2025) · Frontiers in Pharmacology · doi:10.3389/fphar.2025.1562775 · Cited by 2
The Effectiveness of Yoga Exercise on Muscle Strength in the Elderly
Kumara, G. (2022) · INTERNATIONAL JOURNAL OF MULTIDISCIPLINARY RESEARCH AND ANALYSIS · doi:10.47191/ijmra/v5-i8-41 · Cited by 2
Islam, M., & Behura, S. K. (2024) · Genes · doi:10.3390/genes15050604 · Cited by 2
Rhinn, M., Zapata-Bodalo, I., Klein, A., Plassat, J., Knauer-Meyer, T., & Keyes, W. M. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.05.28.446099 · Cited by 2
Xia, K., He, S., Luo, P., Dong, L., Gao, F., Chen, X., Ye, Y., Gao, Y., Ma, Y., Zhang, Y., et al. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.12.11.519976 · Cited by 2
Mazan-Mamczarz, K., Tsitsipatis, D., Carr, A. E., Childs, B. G., Santos, C. R. D., Anerillas, C., Romero, B., Gregg, J. M., Michel, M., Munk, R. B., et al. (2023) · Research Square · doi:10.21203/rs.3.rs-3235572/v1 · Cited by 2
Self-citation
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
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