ArticleAging cell2023
Effect of peripheral cellular senescence on brain aging and cognitive decline.
Article in Aging cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 59 citations in OpenAlex.
- Quercetin Reduces Vascular Senescence and Inflammation in Symptomatic Male but Not Female Coronary Artery Disease Patients.Aging cell · 2025Trial
- The vicious cycle of SASP and inflammaging promotes aging and age-related diseases.Communications biology · 2026Review
- Endogenous neuroprotection in vascular cognitive impairment and dementia.EBioMedicine · 2026Review
- Histone modification dynamics in brain aging: unlocking therapeutic potential.Cell death & disease · 2026Review
- Molecular Mechanisms of Accelerated Ageing in Geriatric Depression: Interplay of Telomere Attrition, Mitochondrial Dysfunction and Cellular Senescence.International journal of molecular sciences · 2026Review
- Context-Dependent Roles of ANGPTL2-Mediated Inflammaging in Tissue Homeostasis, Pathological Tissue Remodeling, and Longevity.Aging cell · 2026Article
- Cognitive-exercise dual-task training delays natural aging/D-galactose-induced cognitive decline in mice.Cellular & molecular biology letters · 2026Article
- Virus-induced endothelial senescence as a cause and driving factor for ME/CFS and long COVID: mediated by a dysfunctional immune system.Cell death & disease · 2026Review
- Neuroinflammation: a critical bridge linking peripheral pathology and age-related degeneration in myasthenia gravis.Frontiers in medicine · 2026Review
- Surgical removal of visceral adipose tissue has therapeutic benefit in male APPFrontiers in endocrinology · 2026Article
- The Yin-Yang of Stress and Senescence: Integrated Stress Response and SASP Crosstalk in Stem Cell Fate, Regeneration, and Disease.Biocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al · 2026Article
- Senotherapeutics for Brain Aging Management.Neurology international · 2025Review
- Pharmacological clearance of senescent cells reduces inflammation, endothelial damage and cardiac fibrosis in HFpEF.Cardiovascular research · 2025Article
- Epigenetic dysregulation of transposable elements in cognitive impairment and Alzheimer's disease.GeroScience · 2025Article
- Immunosenescence in aging and neurodegenerative diseases: evidence, key hallmarks, and therapeutic implications.Translational neurodegeneration · 2025Review
- The Neuroprotective Role of Curcumin: From Molecular Pathways to Clinical Translation-A Narrative Review.Nutrients · 2025Review
- ABT263 Ameliorates Cellular Senescence, Aβ-Dependent Pathology and Cognitive Decline in Aged APP/PS1 Mice via Regulating PI3K/AKT/GSK-3β Pathways.Cell biochemistry and biophysics · 2025Article
- Western Diet and Cognitive Decline: A Hungarian Perspective-Implications for the Design of the Semmelweis Study.Nutrients · 2025Review
- Article
- The senolytic ABT-263 improves cognitive functions in middle-aged male, but not female, atherosclerotic LDLrGeroScience · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
We examine similar and differential effects of two senolytic treatments, ABT-263 and dasatinib + quercetin (D + Q), in preserving cognition, markers of peripheral senescence, and markers of brain aging thought to underlie cognitive decline. Male F344 rats were treated from 12 to 18 months of age with D + Q, ABT-263, or vehicle, and were compared to young (6 months). Both senolytic treatments rescued memory, preserved the blood-brain barrier (BBB) integrity, and prevented the age-related decline in hippocampal N-methyl-D-aspartate receptor (NMDAR) function associated with impaired cognition. Senolytic treatments decreased senescence-associated secretory phenotype (SASP) and inflammatory cytokines/chemokines in the plasma (IL-1β, IP-10, and RANTES), with some markers more responsive to D + Q (TNFα) or ABT-263 (IFNγ, leptin, EGF). ABT-263 was more effective in decreasing senescence genes in the spleen. Both senolytic treatments decreased the expression of immune response and oxidative stress genes and increased the expression of synaptic genes in the dentate gyrus (DG). However, D + Q influenced twice as many genes as ABT-263. Relative to D + Q, the ABT-263 group exhibited increased expression of DG genes linked to cell death and negative regulation of apoptosis and microglial cell activation. Furthermore, D + Q was more effective at decreasing morphological markers of microglial activation. The results indicate that preserved cognition was associated with the removal of peripheral senescent cells, decreasing systemic inflammation that normally drives neuroinflammation, BBB breakdown, and impaired synaptic function. Dissimilarities associated with brain transcription indicate divergence in central mechanisms, possibly due to differential access.
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What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.