Chemotherapy promotes astrocytic response to Aβ deposition, but not Aβ levels, in a mouse model of amyloid and APOE

Ng, Christi Anne S.; Biran, Lucas P; Galvano, Elena; Mandelblatt, Jeanne S.; Vicini, Stefano; Rebeck, G. William

doi:10.1016/j.nbd.2022.105915

Cited by 3 publications

(1 citation statement)

References 77 publications

(94 reference statements)

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“…By employing preclinical models, researchers can also better regulate variables such as age, sex, environmental factors, type of cancer, treatment types, and comorbidities [see review by Seigers et al (182)]. Several recent studies have demonstrated cognitive and neurobiologic deficits in mice treated with doxorubicin, cyclophosphamide, or cisplatin chemotherapy (183)(184)(185)(186)(187)(188). Potential mechanisms of CRCI examined in these studies include sphingosine-1-phosphate receptor 1 activation, brain derived neurotrophic factor levels, apolipoprotein E4 genotype, and neuroinflammation [see review by Gibson and Monje (189)…”

Section: The Role Of Animal Modelsmentioning

confidence: 99%

Neuroimaging based biotypes for precision diagnosis and prognosis in cancer-related cognitive impairment

Kesler,

Henneghan,

Prinsloo

et al. 2023

Front. Med.

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Cancer related cognitive impairment (CRCI) is commonly associated with cancer and its treatments, yet the present binary diagnostic approach fails to capture the full spectrum of this syndrome. Cognitive function is highly complex and exists on a continuum that is poorly characterized by dichotomous categories. Advanced statistical methodologies applied to symptom assessments have demonstrated that there are multiple subclasses of CRCI. However, studies suggest that relying on symptom assessments alone may fail to account for significant differences in the neural mechanisms that underlie a specific cognitive phenotype. Treatment plans that address the specific physiologic mechanisms involved in an individual patient’s condition is the heart of precision medicine. In this narrative review, we discuss how biotyping, a precision medicine framework being utilized in other mental disorders, could be applied to CRCI. Specifically, we discuss how neuroimaging can be used to determine biotypes of CRCI, which allow for increased precision in prediction and diagnosis of CRCI via biologic mechanistic data. Biotypes may also provide more precise clinical endpoints for intervention trials. Biotyping could be made more feasible with proxy imaging technologies or liquid biomarkers. Large cross-sectional phenotyping studies are needed in addition to evaluation of longitudinal trajectories, and data sharing/pooling is highly feasible with currently available digital infrastructures.

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Section: The Role Of Animal Modelsmentioning

confidence: 99%

Neuroimaging based biotypes for precision diagnosis and prognosis in cancer-related cognitive impairment

Kesler,

Henneghan,

Prinsloo

et al. 2023

Front. Med.

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Chemobrain: An accelerated aging process linking adenosine A2A receptor signaling in cancer survivors

Oliveros,

Poleschuk,

Cole

et al. 2023

International Review of Neurobiology

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Alzheimer disease–related biomarkers and cancer-related cognitive decline: the Thinking and Living with Cancer study

Mandelblatt,

Dage,

Zhou

et al. 2024

JNCI: Journal of the National Cancer Institute

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Purpose We evaluated whether plasma Alzheimer’s Disease (AD)-related biomarkers were associated with cancer-related cognitive decline (CRCD) among older breast cancer survivors. Methods We included survivors 60-90 years with primary stage 0-III breast cancers (n = 236) and frequency-matched non-cancer controls (n = 154) who passed a cognitive screen and had banked plasma specimens. Participants were assessed at baseline (pre-systemic therapy) and annually for up to 60-months. Cognition was measured using tests of attention, processing speed and executive function (APE) and learning and memory (LM); perceived cognition was measured by the FACT-Cog PCI. Baseline plasma neurofilament light (NfL), glial fibrillary acidic protein (GFAP), beta-amyloid 42/40 (Aβ42/40) and phosphorylated tau (p-tau181) were assayed using single molecule arrays. Mixed models tested associations between cognition and baseline AD-biomarkers, time, group (survivor vs control) and their two- and three-way interactions, controlling for age, race, WRAT4 Word Reading score, comorbidity and BMI; two-sided 0.05 p-values were considered statistically significant. Results There were no group differences in baseline AD-related biomarkers except survivors had higher baseline NfL levels than controls (p = .013). Survivors had lower adjusted longitudinal APE than controls starting from baseline and continuing over time (p = <0.002). However, baseline AD-related biomarker levels were not independently associated with adjusted cognition over time, except controls had lower APE scores with higher GFAP levels (p = .008). Conclusion The results do not support a relationship between baseline AD-related biomarkers and CRCD. Further investigation is warranted to confirm the findings, test effects of longitudinal changes in AD-related biomarkers and examine other mechanisms and factors affecting cognition pre-systemic therapy.

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Chemotherapy promotes astrocytic response to Aβ deposition, but not Aβ levels, in a mouse model of amyloid and APOE

Cited by 3 publications

References 77 publications

Neuroimaging based biotypes for precision diagnosis and prognosis in cancer-related cognitive impairment

Neuroimaging based biotypes for precision diagnosis and prognosis in cancer-related cognitive impairment

Chemobrain: An accelerated aging process linking adenosine A2A receptor signaling in cancer survivors

Alzheimer disease–related biomarkers and cancer-related cognitive decline: the Thinking and Living with Cancer study

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