ArticleBehavioural brain research2020
A mouse model of chemotherapy-related cognitive impairments integrating the risk factors of aging and APOE4 genotype.
Article in Behavioural brain research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Chemotherapy-Induced Brain Damage: Mechanisms and Insights from Rodent Models.Brain sciences · 2026Review
- APOE4 and doxorubicin impair inhibitory interneuron function and homeostatic regulation in the entorhinal cortex.PloS one · 2026Article
- Advances in neuroimaging in cancer-related cognitive impairment.Frontiers in human neuroscience · 2026Review
- Influence of ApoE genotype on doxorubicin-induced cognitive impairment in juvenile rats.Scientific reports · 2025Article
- Trajectories of Cognitive Complaints in Patients With Breast Cancer and Their Association With Psychosocial and Neurobiological Factors.Cancer medicine · 2025Article
- Perturbations in the neuroactive ligand-receptor interaction and renin angiotensin system pathways are associated with cancer-related cognitive impairment.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2025Article
- Alzheimer disease-related biomarkers and cancer-related cognitive decline: the Thinking and Living with Cancer study.Journal of the National Cancer Institute · 2024Article
- Complications and comorbidities associated with antineoplastic chemotherapy: Rethinking drug design and delivery for anticancer therapy.Acta pharmaceutica Sinica. B · 2024Review
- The chemotherapeutic agent doxorubicin induces brain senescence, with modulation by APOE genotype.Experimental neurology · 2024Article
- Chemobrain: An accelerated aging process linking adenosine AInternational review of neurobiology · 2023Review
- Neuroimaging based biotypes for precision diagnosis and prognosis in cancer-related cognitive impairment.Frontiers in medicine · 2023Review
- Chemotherapy promotes astrocytic response to Aβ deposition, but not Aβ levels, in a mouse model of amyloid and APOE.Neurobiology of disease · 2022Article
- Independent APOE4 knock-in mouse models display reduced brain APOE protein, altered neuroinflammation, and simplification of dendritic spines.Journal of neurochemistry · 2022Article
- Chemobrain in Breast Cancer: Mechanisms, Clinical Manifestations, and Potential Interventions.Drug safety · 2022Review
- Mechanisms of Chemotherapy-Induced Neurotoxicity.Frontiers in pharmacology · 2022Review
- Animal models of chemotherapy-induced cognitive decline in preclinical drug development.Psychopharmacology · 2021Review
- Cancer Chemotherapy Related Cognitive Impairment and the Impact of the Alzheimer's Disease Risk FactorCancers · 2020Review
- Pathogenesis, Assessments, and Management of Chemotherapy-Related Cognitive Impairment (CRCI): An Updated Literature Review.Journal of oncology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Some cancer survivors experience marked cognitive impairment, referred to as cancer-related cognitive impairment (CRCI). CRCI has been linked to the genetic factor APOE4, the strongest genetic risk factor for Alzheimer's disease (AD). We used APOE knock-in mice to test whether the relationship between APOE4 and CRCI can be demonstrated in a mouse model, to identify associations of chemotherapy with behavioural and structural correlates of cognition, and to test whether chemotherapy affects markers of AD. Twelve-month old C57BL/6 J female APOE3 (n = 30) and APOE4 (n = 31) knock-in mice were randomized to treatment with either doxorubicin (10 mg/kg) or saline. Behavioural assays at 2-21 weeks-post exposure included open field maze, elevated zero maze, pre-pulse inhibition, Barnes maze, and fear conditioning. Ex-vivo magnetic resonance imaging was used to determine regional volume differences at 31-35 weeks-post exposure, and tissue sections were analyzed for markers of AD pathogenesis. Minimal toxicities were observed in the aged mice after doxorubicin exposure. In the Barnes maze assay, APOE3 mice did not exhibit impairment in spatial learning after doxorubicin treatment, but APOE4 mice demonstrated significant impairments in both the initial identification of the escape hole and the latency to full escape at 6 weeks post-exposure. Both APOE3 and APOE4 mice treated with doxorubicin showed impairment of spatial memory. Grey matter volume in the frontal cortex decreased in APOE4 mice treated with doxorubicin vs. APOE3 mice. This study demonstrates cognitive impairments in aged APOE4 knock-in mice after doxorubicin treatment and establishes this system as a novel and powerful model of CRCI.
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Registered trials
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