Exosomes from high-altitude cerebral edema patients induce cognitive dysfunction by altering oxidative stress responses in mice.

IF 6.2 1区医学 Q1 PSYCHIATRY

Translational Psychiatry Pub Date : 2025-07-22 DOI:10.1038/s41398-025-03469-2

Qiang Fu, Rui Qiu, Quan Tang, Xiaodong Li, Yaobo Li, Yuxiang Qin, Qiaosheng Li, Jia Yao, Zhongyong Jiang, Huan Xu, Yong Cheng

{"title":"Exosomes from high-altitude cerebral edema patients induce cognitive dysfunction by altering oxidative stress responses in mice.","authors":"Qiang Fu, Rui Qiu, Quan Tang, Xiaodong Li, Yaobo Li, Yuxiang Qin, Qiaosheng Li, Jia Yao, Zhongyong Jiang, Huan Xu, Yong Cheng","doi":"10.1038/s41398-025-03469-2","DOIUrl":null,"url":null,"abstract":"<p><p>The impact of exosomes derived from patients with High Altitude Cerebral Edema (HACE) on cognitive function in mice was investigated, along with the underlying mechanisms. Exosomes were extracted from HACE patients and injected into the dentate gyrus (DG) of mice. A series of behavioral tests assessed cognitive abilities. Results indicated that mice injected with HACE patient exosomes exhibited significant declines in exploratory behavior and object recognition, suggesting notable cognitive impairments. Additionally, these exosomes induced oxidative stress responses and abnormal activation of microglia, closely associated with neuronal death. Proteomic analysis revealed that the differentially expressed protein STAMBP, which is closely linked to neurodevelopment, may play a key role. In conclusion, our findings highlight the potential impact of exosomes from HACE patients on cognitive dysfunction in mice, providing new insights into the pathophysiological mechanisms of HACE.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"15 1","pages":"253"},"PeriodicalIF":6.2000,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12284110/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Translational Psychiatry","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41398-025-03469-2","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"PSYCHIATRY","Score":null,"Total":0}

引用次数: 0

Abstract

The impact of exosomes derived from patients with High Altitude Cerebral Edema (HACE) on cognitive function in mice was investigated, along with the underlying mechanisms. Exosomes were extracted from HACE patients and injected into the dentate gyrus (DG) of mice. A series of behavioral tests assessed cognitive abilities. Results indicated that mice injected with HACE patient exosomes exhibited significant declines in exploratory behavior and object recognition, suggesting notable cognitive impairments. Additionally, these exosomes induced oxidative stress responses and abnormal activation of microglia, closely associated with neuronal death. Proteomic analysis revealed that the differentially expressed protein STAMBP, which is closely linked to neurodevelopment, may play a key role. In conclusion, our findings highlight the potential impact of exosomes from HACE patients on cognitive dysfunction in mice, providing new insights into the pathophysiological mechanisms of HACE.

Abstract Image

查看原文本刊更多论文

高原脑水肿患者的外泌体通过改变小鼠的氧化应激反应诱导认知功能障碍。

研究了来自高原脑水肿（HACE）患者的外泌体对小鼠认知功能的影响及其潜在机制。从HACE患者中提取外泌体并注射到小鼠齿状回（DG）中。一系列的行为测试评估认知能力。结果表明，注射HACE患者外泌体的小鼠在探索行为和物体识别方面表现出明显的下降，表明存在明显的认知障碍。此外，这些外泌体诱导氧化应激反应和小胶质细胞的异常激活，与神经元死亡密切相关。蛋白质组学分析显示，与神经发育密切相关的差异表达蛋白STAMBP可能起关键作用。总之，我们的研究结果强调了HACE患者外泌体对小鼠认知功能障碍的潜在影响，为HACE的病理生理机制提供了新的见解。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Translational Psychiatry PSYCHIATRY-

CiteScore

11.50

自引率

2.90%

发文量

484

审稿时长

23 weeks

期刊介绍： Psychiatry has suffered tremendously by the limited translational pipeline. Nobel laureate Julius Axelrod''s discovery in 1961 of monoamine reuptake by pre-synaptic neurons still forms the basis of contemporary antidepressant treatment. There is a grievous gap between the explosion of knowledge in neuroscience and conceptually novel treatments for our patients. Translational Psychiatry bridges this gap by fostering and highlighting the pathway from discovery to clinical applications, healthcare and global health. We view translation broadly as the full spectrum of work that marks the pathway from discovery to global health, inclusive. The steps of translation that are within the scope of Translational Psychiatry include (i) fundamental discovery, (ii) bench to bedside, (iii) bedside to clinical applications (clinical trials), (iv) translation to policy and health care guidelines, (v) assessment of health policy and usage, and (vi) global health. All areas of medical research, including — but not restricted to — molecular biology, genetics, pharmacology, imaging and epidemiology are welcome as they contribute to enhance the field of translational psychiatry.