ArticleTranslational psychiatry2025
Exosomes from high-altitude cerebral edema patients induce cognitive dysfunction by altering oxidative stress responses in mice.
Article in Translational psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Dnmt3a-mediated abnormal DNA methylation is associated with myelination deficits in offspring of advanced maternal age rats.Molecular biology reports · 2026Article
- Berberine attenuates hyperglycemia induced neurodegeneration in mice by modulation of Nrf2 expression.Molecular biology reports · 2026Article
- Translational stem cell therapy for neurodegeneration and CNS trauma: a focused review.Molecular biology reports · 2026Review
- The CEBPB-AP-1 (JunB/Fos) Axis Drives Neuroinflammation and Microglial Dysfunction Via TNF Signaling in Ischemic Stroke.Inflammation · 2026Article
- Electroacupuncture to point Baihui confers anxiolytic effects by promoting oxytocin release from PVN in Mice.Chinese medicine · 2026Article
- High-Altitude Hypoxia Injury: Systemic Mechanisms and Intervention Strategies on Immune and Inflammatory Responses.Antioxidants (Basel, Switzerland) · 2025Review
- Effects of chronic social defeat stress on behavior and cognition by activating the ERS-NLRP3 signaling pathway in adult mice.Metabolic brain disease · 2025Article
- High-fructose diet induces depressive-like behaviors and short-term memory deficits through hippocampal neurogenesis impairment via neural stem cell dysfunction.Nutrition & metabolism · 2025Article
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Authors and funding
11 authors.
Funding
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.
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