ReviewBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2025
Cognitive dysfunction in chemobrain: Molecular mechanisms and therapeutic implications.
Review in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pathophysiological mechanisms of post-exertional malaise: an integrative analysis based on the metabolism-immune-neuro interaction model.Frontiers in immunology · 2026Pooled it
- Cancer therapy-related cognitive impairment, part 1: an integrative clinical-mechanistic framework from phenotypes to convergent neurobiological pathways.Pharmacological reports : PR · 2026Review
- Working Memory Impairment Induced by Chemotherapy-A Narrative Review.Brain sciences · 2026Review
- A 12-Week Structured Antioxidant-Focused Dietary Intervention Improves Cognitive Function and Oxidative Stress Biomarkers in Lung Cancer Patients with Cancer-Related Cognitive Impairment: A Randomized Controlled Trial.Antioxidants (Basel, Switzerland) · 2026Article
- Evidence-Based Strategies for Addressing Cancer- and Treatment-Related Cognitive Impairment: A Review.Biomolecules & therapeutics · 2026Review
- Physical Exercise Counteracts Impaired Cognition by Improving Mitochondrial Function.International journal of molecular sciences · 2026Review
- Neuroprotective Potential of Encapsulated Pomegranate Peel Polyphenols in Doxorubicin- Induced Neurotoxicity.Plant foods for human nutrition (Dordrecht, Netherlands) · 2026Article
- Sacubitril/Valsartan Fails to Ameliorate Cisplatin-Induced Cognitive Impairment.Drug design, development and therapy · 2026Article
- Mechanisms of natural compounds in treating inhalation anesthesia-induced cognitive dysfunction.Frontiers in pharmacology · 2026Review
- Understanding the distinct role of PI3K(p110Frontiers in cardiovascular medicine · 2026Review
- Chemotherapy-related cognitive impairment as a crisis of the self: a Winnicottian psycho-oncological perspective.Frontiers in psychology · 2026Article
- Impact of Chemotherapy on Motor-Cognitive Dual-Task Performance in Strength and Mobility Tests.Healthcare (Basel, Switzerland) · 2025Article
- Temporal dynamics of cisplatin-induced endothelial senescence and its association with cognitive impairment: insights into the medial prefrontal cortex.Frontiers in oncology · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Chemotherapy-induced cognitive impairment (CICI), commonly referred to as chemobrain, is a prevalent side effect of cancer treatment that severely affects survivors' quality of life. Chemotherapeutic agents, including cisplatin, doxorubicin, and paclitaxel, cross the blood-brain barrier (BBB) and induce neurotoxicity, resulting in cognitive dysfunction. These agents trigger reactive oxygen species (ROS) generation, cause mitochondrial dysfunction, and induce DNA damage, all of which impair synaptic plasticity and neurogenesis. Mitochondrial dysfunction is central to chemobrain, as it disrupts ATP production, increases oxidative stress, and leads to neuronal apoptosis. Furthermore, mitochondrial DNA (mtDNA) damage caused by agents like cisplatin impairs oxidative phosphorylation, exacerbating neuronal degeneration. The molecular mechanisms of chemobrain likely involve several key players, including NAMPT-dependent NAD+ depletion and increased levels of Cyclooxygenase-2 (COX-2), which collectively exacerbate oxidative stress and neuroinflammation. Another important molecular target is the Adenosine A2A receptor (A2AR). When activated, it contributes to synaptic dysfunction and cognitive decline, particularly in chemotherapy-related cognitive deficits in the hippocampus. This review explores the complex interplay of these core pathologies in chemobrain and discusses how targeting these pathways could offer a therapeutic strategy to alleviate cognitive impairments in cancer survivors.
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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.