ArticleFrontiers in aging2025
Epigenetic age acceleration and neurotrophin signaling pathways in cancer-related cognitive impairment: a longitudinal, prospective cohort study.
Article in Frontiers in aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03476070 (Adolescent and Young Adult Cancer Patients), which is not on this map. Cited by 2 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
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.
Adolescent and Young Adult Cancer Patients: Cognitive Toxicity on Survivorship (ACTS)
Who cites it
2 citing papers in PubMed.
- Review
- Multimodal Cancer Therapy and Accelerated Brain Aging: Mechanisms, Biomarkers, and Clinical Consequences.Current oncology (Toronto, Ont.) · 2026Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Biological age acceleration and disruptions in neurotrophin pathway signaling may significantly contribute to cancer-related cognitive impairment (CRCI) etiology. In this study, we evaluated the relationship of epigenetic age acceleration with cognitive function measures and circulating BDNF levels. Furthermore, we evaluated DNA methylation (DNAm) patterns to explore neurotrophin pathway associations with CRCI symptoms. Methods: In a longitudinal study, 51 newly diagnosed Adolescent and Young adult cancer patients and 8 age-matched healthy controls provided blood samples for DNAm and BDNF measurements with concurrent clinical assessments (#NCT03476070). We evaluated the relationship of epigenetic ageing with cancer status, circulating BDNF levels, and measured cognitive function. Next, we identified significant differentially methylated positions (DMPs), regions (DMRs), and significantly enriched pathways associated with BDNF and cognitive function outcomes. Results: PhenoAge and GrimAge demonstrated significant age acceleration relative to non-cancer controls and worsening cognitive function symptoms, with accelerated GrimAge associated with decreasing BDNF levels. DMPs associated with 5 different cognitive function outcomes (FactCog Score, Response, Memory, Executive Function, Multi-Tasking) were mapped to genes within KEGG pathway HSA:04722 (Neurotrophin Signaling Pathway). Key enriched pathways relative to both subjective cognitive function and multiple objective cognitive measurement domains were also enriched with respect to BDNF levels, including Synapse (GO:0045202), Glutamatergic Synapse (GO:0098978), and Neuron Projection (GO:0043005). Conclusion: Cancer and cancer treatment lead to significant epigenetic age acceleration, which can influence neuronal health and CRCI symptom onset. Furthermore, DNAm patterns corroborate BDNF as a potential biomarker for CRCI and suggest neurotrophin pathways play a meaningful role in CRCI etiology.
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Registered trials
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