Chemotherapy-induced cognitive impairment in breast cancer survivors: A systematic review of studies from 2000 to 2021.

BACKGROUND: Studies have indicated that apart from enhancing patient survival, chemotherapy has adverse side effects on the psychological, social, and cognitive functions of breast cancer survivors. AIMS: This study was conducted to understand chemotherapy's impact on breast cancer survivors' cognitive functions. METHODS AND RESULTS: Our study is a systematic review based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. We searched English databases, including PubMed/MEDLINE, PsycINFO, and Web of Science, and Persian databases, such as Irandoc and Elmnet, using Persian keywords of cancer, breast cancer, chemotherapy, cognitive functions, executive functions, and neuropsychological functions. Two reviewers independently evaluated the full text of the articles according to predefined criteria. Among the 937 available studies, 26 were selected based on the inclusion and exclusion criteria, of which 17 (65%) were longitudinal and 9 (35%) were cross-sectional. The findings indicated a significant relationship between the use of chemotherapy and cognitive impairments, most notably attention, working and short-term memory, and executive functions. However, the studies differed in their findings regarding the long-term persistence of cancer-related cognitive impairment (CRCI), which could be due to the wide range of tools used, different methods to measure cognitive functions, and the difference in the sample size of the studies. CONCLUSION: Chemotherapy, affecting cortical and subcortical brain structures, causes a set of cognitive impairments that can lead to impairments in social responsibility acceptance, daily functioning, and quality of life of women. Therefore, rigorous and extensive research design is required to understand the causes and consequences of CRCI using standardized and sensitive measures of cognitive functions. Specifically, studies comparing the effects of different chemotherapy regimens on cognition and potential mechanisms and/or moderators of CRCI would be instrumental in designing more effective therapy regimens and evaluating the efficacy and cost-effectiveness of cognitive rehabilitation and supportive care programs.

Advances of neuroimaging in chemotherapy related cognitive impairment (CRCI) of patients with breast cancer.

BACKGROUND: Chemotherapy related cognitive impairment (CRCI) has seriously affected the quality of life (QOL) of patients with breast cancer (BCs), thus the neurobiological mechanism of CRCI attracted widespread attention. Previous studies have found that chemotherapy causes CRCI through affecting brain structure, function, metabolism, and blood perfusion. FINDINGS: A variety of neuroimaging techniques such as functional magnetic resonance imaging (fMRI), event-related potential (ERP), near-infrared spectroscopy (NIRS) have been widely applied to explore the neurobiological mechanism of CRCI. CONCLUSION: This review summarized the progress of neuroimaging research in BCs with CRCI, which provides a theoretical basis for further exploration of CRCI mechanism, disease diagnosis and symptom intervention in the future. Multiple neuroimaging techniques for CRCI research.

C-phycocyanin Mitigates Cognitive Impairment in Doxorubicin-Induced Chemobrain: Impact on Neuroinflammation, Oxidative Stress, and Brain Mitochondrial and Synaptic Alterations.

Chemotherapy-induced cognitive impairment (CICI) is a common detrimental effect of cancer treatment, occurring in up to 75% of cancer patients. The widely utilized chemotherapeutic agent doxorubicin (DOX) has been implicated in cognitive decline, mostly via cytokine-induced neuroinflammatory and oxidative and mitochondrial damage to brain tissues. C-phycocyanin (CP) has previously been shown to have potent anti-inflammatory, antioxidant, and mitochondrial protective properties. Therefore, this present study was aimed to investigate the neuroprotective effects of CP against DOX-elicited cognitive impairment and explore the underlying mechanisms. CP treatment (50 mg/kg) significantly improved behavioral deficits in DOX-treated mice. Furthermore, CP suppressed DOX-induced neuroinflammation and oxidative stress, mitigated mitochondrial abnormalities, rescued dendritic spine loss, and increased synaptic density in the hippocampus of DOX-treated mice. Our results suggested that CP improves established DOX-induced cognitive deficits, which could be explained at least partly by inhibition of neuroinflammatory and oxidant stress and attenuation of mitochondrial and synaptic dysfunction.