{"title":"衰老和化学脑之间的潜在联系:早期文献综述。","authors":"Nebras Melhem , Shahd Qutifan , Mohammad Alsalem , Tareq Saleh","doi":"10.1016/j.arr.2025.102896","DOIUrl":null,"url":null,"abstract":"<div><div>Chemotherapy-induced cognitive impairment (CICI), commonly referred to as chemobrain, is a pervasive adverse effect of cancer treatment, characterized by deficits in memory, concentration, and executive function. Several observations have suggested a potential for senescence in mediating CICI. First, chemotherapeutic agents that are implicated in CICI can also trigger senescence in neurons and glial cells, accompanied by the senescence-associated secretory phenotype (SASP), that could propagate neuroinflammation, oxidative stress, and synaptic dysfunction. Second, the hippocampus, central to memory and learning, is particularly vulnerable to chemotherapy-induced dendritic spine loss, reduced neurogenesis, and mitochondrial damage and is also a site for senescent cell accumulation. Third, the role of senescence in CICI is further supported by recent studies showing that the selective elimination of senescent cells can mitigate features of CICI. In this work, we attempt to highlight the intricate interplay between the established mechanisms of CICI (oxidative stress, inflammation, DNA damage, and mitochondrial dysfunction) and explore their potential connection to senescence as a central mechanism contributing to CICI. If senescence is then proven to be an established mechanism of CICI, then the use of senolytics or senomorphics could represent novel pharmacological interventions for the treatment of chemobrain.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"112 ","pages":"Article 102896"},"PeriodicalIF":12.4000,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Potential connections between senescence and chemobrain: An early overview of literature\",\"authors\":\"Nebras Melhem , Shahd Qutifan , Mohammad Alsalem , Tareq Saleh\",\"doi\":\"10.1016/j.arr.2025.102896\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Chemotherapy-induced cognitive impairment (CICI), commonly referred to as chemobrain, is a pervasive adverse effect of cancer treatment, characterized by deficits in memory, concentration, and executive function. Several observations have suggested a potential for senescence in mediating CICI. First, chemotherapeutic agents that are implicated in CICI can also trigger senescence in neurons and glial cells, accompanied by the senescence-associated secretory phenotype (SASP), that could propagate neuroinflammation, oxidative stress, and synaptic dysfunction. Second, the hippocampus, central to memory and learning, is particularly vulnerable to chemotherapy-induced dendritic spine loss, reduced neurogenesis, and mitochondrial damage and is also a site for senescent cell accumulation. Third, the role of senescence in CICI is further supported by recent studies showing that the selective elimination of senescent cells can mitigate features of CICI. In this work, we attempt to highlight the intricate interplay between the established mechanisms of CICI (oxidative stress, inflammation, DNA damage, and mitochondrial dysfunction) and explore their potential connection to senescence as a central mechanism contributing to CICI. If senescence is then proven to be an established mechanism of CICI, then the use of senolytics or senomorphics could represent novel pharmacological interventions for the treatment of chemobrain.</div></div>\",\"PeriodicalId\":55545,\"journal\":{\"name\":\"Ageing Research Reviews\",\"volume\":\"112 \",\"pages\":\"Article 102896\"},\"PeriodicalIF\":12.4000,\"publicationDate\":\"2025-09-10\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Ageing Research Reviews\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1568163725002429\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Ageing Research Reviews","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1568163725002429","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
Potential connections between senescence and chemobrain: An early overview of literature
Chemotherapy-induced cognitive impairment (CICI), commonly referred to as chemobrain, is a pervasive adverse effect of cancer treatment, characterized by deficits in memory, concentration, and executive function. Several observations have suggested a potential for senescence in mediating CICI. First, chemotherapeutic agents that are implicated in CICI can also trigger senescence in neurons and glial cells, accompanied by the senescence-associated secretory phenotype (SASP), that could propagate neuroinflammation, oxidative stress, and synaptic dysfunction. Second, the hippocampus, central to memory and learning, is particularly vulnerable to chemotherapy-induced dendritic spine loss, reduced neurogenesis, and mitochondrial damage and is also a site for senescent cell accumulation. Third, the role of senescence in CICI is further supported by recent studies showing that the selective elimination of senescent cells can mitigate features of CICI. In this work, we attempt to highlight the intricate interplay between the established mechanisms of CICI (oxidative stress, inflammation, DNA damage, and mitochondrial dysfunction) and explore their potential connection to senescence as a central mechanism contributing to CICI. If senescence is then proven to be an established mechanism of CICI, then the use of senolytics or senomorphics could represent novel pharmacological interventions for the treatment of chemobrain.
期刊介绍:
With the rise in average human life expectancy, the impact of ageing and age-related diseases on our society has become increasingly significant. Ageing research is now a focal point for numerous laboratories, encompassing leaders in genetics, molecular and cellular biology, biochemistry, and behavior. Ageing Research Reviews (ARR) serves as a cornerstone in this field, addressing emerging trends.
ARR aims to fill a substantial gap by providing critical reviews and viewpoints on evolving discoveries concerning the mechanisms of ageing and age-related diseases. The rapid progress in understanding the mechanisms controlling cellular proliferation, differentiation, and survival is unveiling new insights into the regulation of ageing. From telomerase to stem cells, and from energy to oxyradical metabolism, we are witnessing an exciting era in the multidisciplinary field of ageing research.
The journal explores the cellular and molecular foundations of interventions that extend lifespan, such as caloric restriction. It identifies the underpinnings of manipulations that extend lifespan, shedding light on novel approaches for preventing age-related diseases. ARR publishes articles on focused topics selected from the expansive field of ageing research, with a particular emphasis on the cellular and molecular mechanisms of the aging process. This includes age-related diseases like cancer, cardiovascular disease, diabetes, and neurodegenerative disorders. The journal also covers applications of basic ageing research to lifespan extension and disease prevention, offering a comprehensive platform for advancing our understanding of this critical field.