ReviewAging and disease2025
Mechanistic Role of Astrocytic Rac1 Protein in Alzheimer's Disease.
Review in Aging and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Dysfunctional astrocytes regulate excitatory neurons via cell adhesion and vascular lesions in patients with Alzheimer's disease.Journal of translational medicine · 2026Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The prevalence of Alzheimer's disease (AD) has been increasing worldwide due to the aging population, placing a substantial burden on both society and families. To date, the underlying pathogenesis of AD has not been comprehensively elucidated, and advancements in drug development for this disease have been relatively slow. Astrocytes are crucial for maintaining the homeostasis of the brain microenvironment. Astrocyte dysfunction has been closely linked to AD onset and progression. The Rac1 protein, which belongs to the Rho GTPase family, exhibits hyperactivation in the astrocytes of AD model mice. Nevertheless, the exact role of Rac1 in the pathogenesis of AD remains ambiguous. The TLR4/Rac1/NLRP3 signaling pathway is involved in diverse cellular activities and inflammatory responses and plays a significant role in the AD neuroinflammatory process. This review explores the mechanism of action of Rac1 in astrocytes in the context of AD and how the TLR4/Rac1/NLRP3 pathway influences the pathological process, offering novel theoretical foundations and potential therapeutic targets for preventing and treating this disease.
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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.