ArticleNeurobiology of disease2022
Chemotherapy promotes astrocytic response to Aβ deposition, but not Aβ levels, in a mouse model of amyloid and APOE.
Article in Neurobiology of disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Neuroglia Alterations in the Olfactory Bulbs in Patients with Schizophrenia: An Exploratory Postmortem Study.Life (Basel, Switzerland) · 2026Article
- Tumor-derived apolipoprotein E confers resistance to temozolomide in pancreatic neuroendocrine tumors.Cell death & disease · 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
- Neuroimaging based biotypes for precision diagnosis and prognosis in cancer-related cognitive impairment.Frontiers in medicine · 2023Review
- Chemobrain: An accelerated aging process linking adenosine AInternational review of neurobiology · 2023Review
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
Many cancer survivors experience cancer-related cognitive impairment (CRCI), which is characterized by problems of attention, working memory, and executive function following chemotherapy and/or hormonal treatment. APOE4, the strongest genetic risk factor for Alzheimer's Disease (AD), is also a risk factor for CRCI, especially among survivors exposed to chemotherapy. We explored whether the effects of APOE genotype to chemotherapy were associated with an increase in AD pathological processes, using a mouse model of amyloid (5XFAD) along with the E3 or E4 alleles of human APOE (E3FAD and E4FAD). Six-month-old female E3FAD mice (control n = 5, treated n = 5) and E4FAD (control n = 6, treated n = 6) were treated with two doses of doxorubicin (total 10 mg/kg) or DMSO vehicle. After six weeks, mice were euthanized and brains were analyzed by immunohistochemistry and biochemical assays. Doxorubicin-treated mice had the same level of Aβ in the brain as control mice, as measured by 6E10 immunohistochemistry, Aβ40 and Aβ42 ELISAs, and plaque morphologies. Doxorubicin significantly increased the level of the astrocytic response to Aβ deposits, which was independent of APOE genotype; no effects of doxorubicin were observed on the microglial responses. These data are consistent with a model in which the effects of doxorubicin on risk of CRCI are unrelated amyloid accumulation, but possibly related to glial responses to damage.
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