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

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 tes...

Full description

Saved in:
Bibliographic Details
Main Authors: Qiang Fu, Rui Qiu, Quan Tang, Xiaodong Li, Yaobo Li, Yuxiang Qin, Qiaosheng Li, Jia Yao, Zhongyong Jiang, Huan Xu, Yong Cheng
Format: Article
Language:English
Published: Nature Publishing Group 2025-07-01
Series:Translational Psychiatry
Online Access:https://doi.org/10.1038/s41398-025-03469-2
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849332016865083392
author Qiang Fu
Rui Qiu
Quan Tang
Xiaodong Li
Yaobo Li
Yuxiang Qin
Qiaosheng Li
Jia Yao
Zhongyong Jiang
Huan Xu
Yong Cheng
author_facet Qiang Fu
Rui Qiu
Quan Tang
Xiaodong Li
Yaobo Li
Yuxiang Qin
Qiaosheng Li
Jia Yao
Zhongyong Jiang
Huan Xu
Yong Cheng
author_sort Qiang Fu
collection DOAJ
description 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.
format Article
id doaj-art-bf668b13a55b4961ae8ebba84f770c1f
institution Kabale University
issn 2158-3188
language English
publishDate 2025-07-01
publisher Nature Publishing Group
record_format Article
series Translational Psychiatry
spelling doaj-art-bf668b13a55b4961ae8ebba84f770c1f2025-08-20T03:46:21ZengNature Publishing GroupTranslational Psychiatry2158-31882025-07-0115111210.1038/s41398-025-03469-2Exosomes from high-altitude cerebral edema patients induce cognitive dysfunction by altering oxidative stress responses in miceQiang Fu0Rui Qiu1Quan Tang2Xiaodong Li3Yaobo Li4Yuxiang Qin5Qiaosheng Li6Jia Yao7Zhongyong Jiang8Huan Xu9Yong Cheng10Institute of National Security, Center on Translational Neuroscience, Minzu University of ChinaInstitute of National Security, Center on Translational Neuroscience, Minzu University of ChinaCollege of Life and Environmental Sciences, Minzu University of ChinaCollege of Life and Environmental Sciences, Minzu University of ChinaCollege of Life and Environmental Sciences, Minzu University of ChinaCollege of Life and Environmental Sciences, Minzu University of ChinaCollege of Life and Environmental Sciences, Minzu University of ChinaCollege of Life and Environmental Sciences, Minzu University of ChinaDepartment of Medical Laboratory, Affiliated Cancer Hospital of Chengdu Medical College, Chengdu Seventh People’s HospitalDepartment of Clinical Laboratory, General Hospital of Xizang Military CommandInstitute of National Security, Center on Translational Neuroscience, Minzu University of ChinaAbstract 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.https://doi.org/10.1038/s41398-025-03469-2
spellingShingle Qiang Fu
Rui Qiu
Quan Tang
Xiaodong Li
Yaobo Li
Yuxiang Qin
Qiaosheng Li
Jia Yao
Zhongyong Jiang
Huan Xu
Yong Cheng
Exosomes from high-altitude cerebral edema patients induce cognitive dysfunction by altering oxidative stress responses in mice
Translational Psychiatry
title Exosomes from high-altitude cerebral edema patients induce cognitive dysfunction by altering oxidative stress responses in mice
title_full Exosomes from high-altitude cerebral edema patients induce cognitive dysfunction by altering oxidative stress responses in mice
title_fullStr Exosomes from high-altitude cerebral edema patients induce cognitive dysfunction by altering oxidative stress responses in mice
title_full_unstemmed Exosomes from high-altitude cerebral edema patients induce cognitive dysfunction by altering oxidative stress responses in mice
title_short Exosomes from high-altitude cerebral edema patients induce cognitive dysfunction by altering oxidative stress responses in mice
title_sort exosomes from high altitude cerebral edema patients induce cognitive dysfunction by altering oxidative stress responses in mice
url https://doi.org/10.1038/s41398-025-03469-2
work_keys_str_mv AT qiangfu exosomesfromhighaltitudecerebraledemapatientsinducecognitivedysfunctionbyalteringoxidativestressresponsesinmice
AT ruiqiu exosomesfromhighaltitudecerebraledemapatientsinducecognitivedysfunctionbyalteringoxidativestressresponsesinmice
AT quantang exosomesfromhighaltitudecerebraledemapatientsinducecognitivedysfunctionbyalteringoxidativestressresponsesinmice
AT xiaodongli exosomesfromhighaltitudecerebraledemapatientsinducecognitivedysfunctionbyalteringoxidativestressresponsesinmice
AT yaoboli exosomesfromhighaltitudecerebraledemapatientsinducecognitivedysfunctionbyalteringoxidativestressresponsesinmice
AT yuxiangqin exosomesfromhighaltitudecerebraledemapatientsinducecognitivedysfunctionbyalteringoxidativestressresponsesinmice
AT qiaoshengli exosomesfromhighaltitudecerebraledemapatientsinducecognitivedysfunctionbyalteringoxidativestressresponsesinmice
AT jiayao exosomesfromhighaltitudecerebraledemapatientsinducecognitivedysfunctionbyalteringoxidativestressresponsesinmice
AT zhongyongjiang exosomesfromhighaltitudecerebraledemapatientsinducecognitivedysfunctionbyalteringoxidativestressresponsesinmice
AT huanxu exosomesfromhighaltitudecerebraledemapatientsinducecognitivedysfunctionbyalteringoxidativestressresponsesinmice
AT yongcheng exosomesfromhighaltitudecerebraledemapatientsinducecognitivedysfunctionbyalteringoxidativestressresponsesinmice