ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Tau Pathology Drives Disease-Associated Astrocyte Reactivity in Salt-Induced Neurodegeneration.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Comorbid mechanisms of neuroinflammation and astrocytic ferroptosis in neurological disorders: A vicious cycle (Review).Biomedical reports · 2026Review
- Impact of High Dietary Salt on Neurovascular and Cognitive Functions.Hypertension (Dallas, Tex. : 1979) · 2026Review
- RRx-001 ameliorates astrocyte pyroptosis by regulating LCN2-NLRP3 inflammasome activation in an MPTP-induced parkinson's disease mouse model.Cellular and molecular life sciences : CMLS · 2026Article
- Limettin and PD98059 Mitigated Alzheimer's Disease Like Pathology Induced by Streptozotocin in Mouse Model: Role of p-ERK1/2/p-GSK-3β/p-CREB/BDNF Pathway.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Tau Pathology Drives Disease-Associated Astrocyte Reactivity in Salt-Induced Neurodegeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Dietary high salt intake is increasingly recognized as a risk factor for cognitive decline and dementia, including Alzheimer's disease (AD). Recent studies have identified a population of disease-associated astrocytes (DAA)-like astrocytes closely linked to amyloid deposition and tau pathology in an AD mouse model. However, the presence and role of these astrocytes in high-salt diet (HSD) models remain unexplored. In this study, it is demonstrated that HSD significantly induces enhanced reactivity of DAA-like astrocytes in the hippocampal CA3 region of mice, with this reactivity being critically dependent on neuronal tau pathology. Neuronal tau pathology activates adenosine A1R signaling, exacerbating tau pathology by inhibiting the Cers1 pathway, which sustains astrocyte reactivity. Additionally, neurons burdened with tau pathology promote astrocyte reactivity via releasing Proteins Associated with Promoting DAA-like Astrocyte Reactivity (PAPD), with Lcn2 playing a pivotal role. Knockout of Lcn2 or its receptor 24p3R significantly mitigates HSD-induced DAA reactivity and neuroinflammation. These findings suggest a vicious cycle between tau pathology and A1R signaling, driving DAA-like astrocyte reactivity. Targeting the Tau-A1R axis may provide a novel therapeutic strategy for reducing HSD-induced neuroinflammation and cognitive deficits.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.