ArticleFrontiers in cellular and infection microbiology2025
The amyloid-beta wave hypothesis of Alzheimer's disease.
Article in Frontiers in cellular and infection microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- GPER in murine astrocytes and mural cells promotes neurovascular coupling and Aβ clearance.Research square · 2026Article
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4 authors.
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Abstract
Alzheimer's disease (AD) is a complex and multifactorial disorder that affects all races and genders. Genetic traits influenced by lifestyle and environment lead to a tremendous amount of heterogeneity in Alzheimer's disease onset and severity. Regardless of these unique contributing factors, Alzheimer's disease is traditionally met with amyloid-beta plaque formation in the central nervous system. In this commentary, we shed light on the growing literature surrounding amyloid-beta's ability to act as an antimicrobial peptide in the central nervous system's innate immune response to pathogenic infections. We hypothesize that there are, "amyloid-beta waves" that are created by the responses of neuroglia and neurons to microbial pathogens. The improper clearance and residual buildup of amyloid-beta waves throughout life increases the likelihood of developing Alzheimer's disease. In conclusion, we suggest that anti-amyloid therapies during pathogenic infections or flare-ups may slow the development of Alzheimer's disease by reducing amyloid-beta waves throughout the aging of individuals.
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