ArticleAging cell2023
Accelerated cerebromicrovascular senescence contributes to cognitive decline in a mouse model of paclitaxel (Taxol)-induced chemobrain.
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 62 papers, 3 of them syntheses that pooled it.
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Who cites it
62 citing papers in PubMed, 3 syntheses or guidelines pooled it, 82 citations in OpenAlex.
- Chemotherapy-related cognitive impairment and non-pharmacological interventions targeting the nervous system: a systematic review.Frontiers in psychiatry · 2026Pooled it
- The risk of dementia in breast cancer survivors: a meta-analysis of observational studies.Annals of medicine · 2025Pooled it
- Incidence and influencing factors of chemotherapy-induced peripheral neuropathy in cancer patients: a systematic review and meta-analysis.Frontiers in neurologyPooled it
- Long-term cerebrovascular effects of cyclophosphamide and vincristine: endothelial senescence, impaired DNA repair signaling, and blood-brain barrier dysfunction.GeroScience · 2026Article
- Cancer therapy-related cognitive impairment, part 1: an integrative clinical-mechanistic framework from phenotypes to convergent neurobiological pathways.Pharmacological reports : PR · 2026Review
- Targeting cellular senescence mitigates chemotherapy-induced bone loss in young and aged mice.GeroScience · 2026Article
- Chemotherapy-Induced Brain Damage: Mechanisms and Insights from Rodent Models.Brain sciences · 2026Review
- Chemotherapy neurotoxicity and aging: Uncovering shared central nervous system pathologies and potential interventions.Neuro-oncology advances · 2026Review
- Tumour endothelial cell reprogramming orchestrates angiocrine signalling to drive chemoresistance in breast cancer.Angiogenesis · 2026Article
- A Age Related Vascular Senescence: Mystery of Blood-brain Barrier Dysfunction in Neurodegeneration.Molecular neurobiology · 2026Review
- Multi-contrast optical coherence tomography forBiomedical optics express · 2026Article
- Article
- Exploration of the mechanism of chemobrain related to neuroinflammation from 1994 to 2023.Clinics (Sao Paulo, Brazil) · 2026Review
- The immune-endothelial axis in neurovascular pathophysiology: a framework for targeted interventions.Frontiers in immunology · 2026Review
- Metabolomics-based exploration of the pathogenesis of breast cancer-related fatigue and progress of traditional Chinese medicine intervention.Frontiers in oncology · 2026Review
- Mild traumatic brain injury promotes chronic cerebrovascular inflammation and glymphatic suppression.Molecular neurodegeneration advances · 2026Article
- Smartphone-Based Physical Activity Program to Reduce "Chemo-Brain" Symptoms and Improve Health in Cancer Survivors With and Without Type 2 Diabetes: Protocol for a Single-Arm Pre-Post Pilot Trial.JMIR research protocols · 2025Article
- The effects of doxorubicin on blood-brain barrier integrity in hCMEC/D3.Neurotoxicology · 2025Article
- Mechanisms and treatment of cancer therapy-induced peripheral and central neurotoxicity.Nature reviews. Cancer · 2025Review
- Frequency, patient characteristics, and clinical management for extravasation with docetaxel: a descriptive study using a large Japanese medical claims database.Journal of pharmaceutical health care and sciences · 2025Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 4 institutions in 2 countries.
Funding
Abstract
Chemotherapy-induced cognitive impairment ("chemobrain") is a frequent side-effect in cancer survivors treated with paclitaxel (PTX). The mechanisms responsible for PTX-induced cognitive impairment remain obscure, and there are no effective treatments or prevention strategies. Here, we test the hypothesis that PTX induces endothelial senescence, which impairs microvascular function and contributes to the genesis of cognitive decline. We treated transgenic p16-3MR mice, which allows the detection and selective elimination of senescent cells, with PTX (5 mg/kg/day, 2 cycles; 5 days/cycle). PTX-treated and control mice were tested for spatial memory performance, neurovascular coupling (NVC) responses (whisker-stimulation-induced increases in cerebral blood flow), microvascular density, blood-brain barrier (BBB) permeability and the presence of senescent endothelial cells (by flow cytometry and single-cell transcriptomics) at 6 months post-treatment. PTX induced senescence in endothelial cells, which associated with microvascular rarefaction, NVC dysfunction, BBB disruption, neuroinflammation, and impaired performance on cognitive tasks. To establish a causal relationship between PTX-induced senescence and impaired microvascular functions, senescent cells were depleted from PTX-treated animals (at 3 months post-treatment) by genetic (ganciclovir) or pharmacological (treatment with the senolytic drug ABT263/Navitoclax) means. In PTX treated mice, both treatments effectively eliminated senescent endothelial cells, rescued endothelium-mediated NVC responses and BBB integrity, increased capillarization and improved cognitive performance. Our findings suggest that senolytic treatments can be a promising strategy for preventing chemotherapy-induced cognitive impairment.
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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 OpenQuestion graph.