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Chemotherapy-related cognitive impairment (CRCI) is a prevalent and distressing issue among older adults with cancer, affecting quality of life and treatment adherence. While its mechanisms remain unclear, biomarkers have emerged as promising tools for understanding CRCI. This systematic review aimed to explore the relationships between cognitive impairment following chemotherapy and biomarkers in older patients with cancer. A comprehensive search was conducted through December 2024 across PubMed, CINAHL, Embase, PsycINFO, and the Cochrane Library. An additional hand search was performed through July 2025. The focus was on patients over 60 years old with chemotherapy-related cognitive impairment and associated biomarkers. The review adhered to PRISMA 2020 guidelines, and the methodological quality of included studies was assessed using the Joanna Briggs Institute checklist to ensure rigor and reliability. Six of the initial 6,324 articles met the inclusion criteria, and seven additional studies were identified through manual searching. In total, 13 studies identified several biomarkers associated with CRCI in older patients with cancer. These included serum hemoglobin, brain-derived neurotrophic factor, percent cerebral oxyhemoglobin, functional network connectivity, and individual alpha peak frequency. This review highlights several biomarkers potentially associated with CRCI in older patients with cancer, though consistent and definitive biomarkers remain elusive. Further research is needed to clarify the biological mechanisms underlying CRCI and inform the development of interventions aimed at preventing cognitive decline in this vulnerable population. The identification of validated biomarkers will be critical for advancing personalized nursing and improving clinical outcomes in older adults with cancer. Show less

Chemotherapy-induced peripheral neuropathy (CIPN) remains a major unmet challenge in oncology, affecting treatment adherence and patient quality of life. Despite its prevalence, reliable predictive biomarkers and targeted neuroprotective strategies remain elusive. This study integrates clinical data, whole-genome sequencing, and translational research to identify genetic determinants of CIPN susceptibility and validate therapeutic approaches. Through comprehensive analysis of patients with colorectal cancer, including neurophysiological evaluations and CIPN-specific quality-of-life assessments, we identified the Show less

Women face a heightened risk of Alzheimer's disease (AD), partly attributed to post-menopausal estrogen loss. Given that ERβ activation avoids the oncogenic risks of ERα and GPR40 plays a pivotal role in neuronal function, the ERβ/GPR40 axis show a promising therapeutic target for anti-AD drug discovery. To inspect the role of this axis, we employed Vincamine (Vin), a monoterpenoid indole alkaloid from Madagascar periwinkle that we previously identified as a GPR40 agonist. To elucidate the role of ERβ/GPR40 axis in AD pathogenesis and to investigate the therapeutic potential of Vin in ameliorating AD-related deficits. We combined analyses of clinical data from female AD patients (GSE33000) with the research in 3×Tg-AD mice to examine the differences in ERβ/GPR40 expression. The binding of ERβ and GPR40 was detected by CUT&Tag assay, protein-DNA docking simulation and molecular dynamics simulation assays. Vin was used to evaluate the therapeutic potential of ERβ/GPR40 axis activation for AD. The underlying mechanisms were investigated by assay against the adeno-associated virus (AAV)-CMV-PHP.eB-KD-GPR40 injected 3×Tg-AD female mice. ERβ and GPR40 are both downregulated in brains of female AD patients and 3×Tg-AD mice, and ERβ directly binds to GPR40 promoter. Brain-specific GPR40 knockdown caused cognitive impairment in female wild type (WT) mice. Vin as a GPR40 agonist but not an ERβ ligand ameliorated AD-like pathology in 3×Tg-AD female mice. Specifically, Vin suppressed neuroinflammation via GPR40/NF-κB/NLRP3 pathway, inhibited neuronal tau hyperphosphorylation via GPR40/GSK3β/CaMKII pathway, while promoted synaptic plasticity via GPR40/PKA/CREB/BDNF pathway. To our knowledge, our study provides the first identification of the specific ERβ-binding regions and key residues within the GPR40 promoter, offering novel mechanistic insight into their transcriptional regulation. Furthermore, our work establishes ERβ/GPR40 axis as a potentially therapeutic strategy for female AD and highlight the medication interest of Vin in treating this disease. Show less