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Tau Pathology Drives Disease‐Associated Astrocyte Reactivity in Salt‐Induced Neurodegenerationстатья Исследовательская статья
Статья опубликована в высокорейтинговом журнале
Статья опубликована в журнале из списка Web of Science и/или Scopus- Авторы: Tong‐Yu Rui, He‐Zhou Huang, Kai Zheng, Hong‐Wei Fan, Juan Zhang, Zi‐Yuan Guo, Heng‐Ye Man, Nadezhda Brazhe, Alexey Semyanov, You‐Ming Lu, Dan Liu, Ling‐Qiang Zhu
- Журнал: Advanced Science
- Том: 12
- Номер: 11
- Год издания: 2025
- Издательство: Wiley-Blackwell
- Местоположение издательства: United States
- Номер статьи: 2410799
- DOI: 10.1002/advs.202410799
- Аннотация: Dietary high salt intake is increasingly recognized as a risk factor for cognitivedecline and dementia, including Alzheimer’s disease (AD). Recent studieshave identified a population of disease-associated astrocytes (DAA)-likeastrocytes closely linked to amyloid deposition and tau pathology in an ADmouse model. However, the presence and role of these astrocytes in high-saltdiet (HSD) models remain unexplored. In this study, it is demonstrated thatHSD significantly induces enhanced reactivity of DAA-like astrocytes in thehippocampal CA3 region of mice, with this reactivity being criticallydependent on neuronal tau pathology. Neuronal tau pathology activatesadenosine A1R signaling, exacerbating tau pathology by inhibiting the Cers1pathway, which sustains astrocyte reactivity. Additionally, neurons burdenedwith tau pathology promote astrocyte reactivity via releasing ProteinsAssociated with Promoting DAA-like Astrocyte Reactivity (PAPD), with Lcn2playing a pivotal role. Knockout of Lcn2 or its receptor 24p3R significantlymitigates HSD-induced DAA reactivity and neuroinflammation. Thesefindings suggest a vicious cycle between tau pathology and A1R signaling,driving DAA-like astrocyte reactivity. Targeting the Tau-A1R axis may provide anovel therapeutic strategy for reducing HSD-induced neuroinflammation andcognitive deficits.
- Добавил в систему: Браже Надежда Александровна
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