时间标签：数据日期 2026-10-31 · 生成时间 2026-11-01 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/28–2026/10/31 ｜ 情报发生日期 2026-10-31
研究问题
However, these mechanisms alone do not fully explain the considerable variability in the onset, severity, and persistence of cognitive dysfunction observed among patients.；However, persistent or severe chemotherapeutic stress may overwhelm these compensatory mechanisms, resulting in maladaptive mitochondrial remodeling, characterized by defective mitochondrial quality control, sustained oxidative stress, chronic neuroinflammation, and progressive neuronal dysfunction [, , ].；Despite these advances, direct mechanistic evidence linking chemotherapy‐induced gut dysbiosis, mitochondrial reprogramming, and cognitive impairment remains relatively limited.
方法
These factors profoundly remodel the tissue microenvironment and promote a state of chronic, low‐grade inflammation (“inflammaging”), thereby reinforcing senescence in neighboring cells and sustaining inflammatory signaling networks.；Activated microglia adopt a proinflammatory phenotype, sustaining the production of cytokines and neurotoxic mediators, thereby perpetuating chronic neuroinflammation [, ].；A randomized controlled trial suggests that probiotic supplementation may improve cognitive performance in patients with breast cancer receiving chemotherapy [].
核心结论
Chemotherapy‐induced cognitive impairment (CICI), commonly referred to as chemobrain, is increasingly recognized as a significant clinical complication among cancer survivors, particularly as advances in cancer treatment continue to improve long‐term survival.；CICI is characterized by impairments in memory, attention, executive function, and processing speed, which may develop during chemotherapy and persist for months or even years after treatment, substantially affecting daily functioning and quality of life [, ].；Collectively, these findings suggest that additional interconnected biological processes contribute to the development and progression of CICI. ‖ 结论：Viewing CICI from this perspective highlights the complex interplay between systemic and central pathways while also identifying key targets for therapeutic intervention.
局限
Future research should focus on translating these mechanistic insights into clinically relevant interventions.
对本项目的价值
★☆☆☆☆ 脑老化是最大未满足需求，也是终点最难量化的领域；biomarker 与认知读数选择最敏感。
全文来源
PMC JATS 全文（正文 45,498 字符，已过标题/DOI 逐字归属校验）
原文题录
- 英文标题：Mitochondrial Reprogramming Along the Gut-Brain Axis in Chemotherapy-Induced Cognitive Impairment: A Narrative Review.
- 期刊与标识：Oxid Med Cell Longev · PMID 42949236 · DOI 10.1155/omcl/5350976
C 级证据分级：C 级（预印本 / 观点评论，非原始研究）
本文属观点/评论类文献，不是原始研究。其论点依赖于作者对既有证据的梳理与判断，不构成新的实验证据。本站标注 C 级即为此意——阅读时请把它当作「领域内的思考框架」，而非「研究发现」。
关于本文的文献来源：本站依据 IMA 知识库「五刊监控·深度文献卡片」撰写，依据已获取的期刊全文（方法、样本量与结论已回到原文核对）；未能获取全文的同批条目另行标注「摘要级」，全程未做任何数值推算补全。