ArticleAging cell2024
Senolytic treatment alleviates doxorubicin-induced chemobrain.
Article in Aging cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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
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Who cites it
20 citing papers in PubMed, 24 citations in OpenAlex.
- Chemotherapy neurotoxicity and aging: Uncovering shared central nervous system pathologies and potential interventions.Neuro-oncology advances · 2026Review
- Mechanistic Insights into metformin's neuroprotective effects against drug-induced neurotoxicity.Metabolic brain disease · 2026Review
- A Age Related Vascular Senescence: Mystery of Blood-brain Barrier Dysfunction in Neurodegeneration.Molecular neurobiology · 2026Review
- Mechanistic insights and therapeutic interventions of mitochondrial quality control in chemotherapy-related cognitive impairment.Neoplasia (New York, N.Y.) · 2026Review
- Multimodal Cancer Therapy and Accelerated Brain Aging: Mechanisms, Biomarkers, and Clinical Consequences.Current oncology (Toronto, Ont.) · 2026Review
- Revolutionizing cancer treatment with senotherapeutics: a current perspective.Cancer chemotherapy and pharmacology · 2026Review
- APOE4 and doxorubicin impair inhibitory interneuron function and homeostatic regulation in the entorhinal cortex.PloS one · 2026Article
- Prodrug nanoplatform for triggering ferroptosis to eliminate senescent cells in age-associated pathologies.Nature communications · 2025Article
- Single-Nucleus RNA Sequencing of HDAC6 Inhibition in Resolving Doxorubicin-Induced Cognitive Impairment.Molecular neurobiology · 2025Article
- Ameliorative effects of agomelatine against doxorubicin-induced hepatotoxicity.BMC pharmacology & toxicology · 2025Article
- Western Diet and Cognitive Decline: A Hungarian Perspective-Implications for the Design of the Semmelweis Study.Nutrients · 2025Review
- The senolytic ABT-263 improves cognitive functions in middle-aged male, but not female, atherosclerotic LDLrGeroScience · 2025Article
- The adverse effects of chemotherapy on bone mass are not prevented by senolytics.Scientific reports · 2025Article
- The chemotherapy agent doxorubicin induces CNS expression of Ascl1, a regulator of adult neurogenesis and differentiation.Scientific reports · 2025Article
- Sex, senescence, senolytics, and cognition.Frontiers in aging neuroscience · 2025Review
- Article
- A Conversation with ChatGPT on Contentious Issues in Senescence and Cancer Research.Molecular pharmacology · 2024Article
- Therapy-induced senescence is finally escapable, what is next?Cell cycle (Georgetown, Tex.) · 2024Review
- Senolytic treatment alleviates doxorubicin-induced chemobrain.Aging cell · 2024Article
- Failure of senolytic treatment to prevent cognitive decline in a female rodent model of aging.Frontiers in aging neuroscience · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Doxorubicin (Dox), a widely used treatment for cancer, can result in chemotherapy-induced cognitive impairments (chemobrain). Chemobrain is associated with inflammation and oxidative stress similar to aging. As such, Dox treatment has also been used as a model of aging. However, it is unclear if Dox induces brain changes similar to that observed during aging since Dox does not readily enter the brain. Rather, the mechanism for chemobrain likely involves the induction of peripheral cellular senescence and the release of senescence-associated secretory phenotype (SASP) factors and these SASP factors can enter the brain to disrupt cognition. We examined the effect of Dox on peripheral and brain markers of aging and cognition. In addition, we employed the senolytic, ABT-263, which also has limited access to the brain. The results indicate that plasma SASP factors enter the brain, activating microglia, increasing oxidative stress, and altering gene transcription. In turn, the synaptic function required for memory was reduced in response to altered redox signaling. ABT-263 prevented or limited most of the Dox-induced effects. The results emphasize a link between cognitive decline and the release of SASP factors from peripheral senescent cells and indicate some differences as well as similarities between advanced age and Dox treatment.
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What OpenQuestion 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 OpenQuestion graph.