ArticleMolecular neurobiology2025
A Ginsenoside Composition Ameliorated Aβ and Tau Aggregation via Autophagy Lysosome Pathway.
Article in Molecular neurobiology, 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.
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized by the abnormal deposition of amyloid-beta (Aβ) peptides and neurofibrillary tangles (NFTs). Ginsenosides, the primary active constituents in ginseng, exhibit potential in combating AD. In our previous work, the ginsenoside SumI was demonstrated to have superior anti-AD activity compared to other ginsenosides when used alone. This study revealed that SumI effectively decreased the lysosomal pH, promoted autophagosome formation, increased autophagic flux, and facilitated the transport of misfolded proteins to lysosomes for degradation in Caenorhabditis elegans. SumI activated the HLH-30 transcription factor by triggering a lipid-catabolic response akin to starvation. bec-1 RNAi significantly abrogated the anti-AD effect of SumI. Our findings indicate that SumI mitigated protein aggregation by activating the autophagy-lysosome pathway in C. elegans and provide scientific evidence that ginsenoside composition could be a potential therapeutic agent for treating or preventing AD.
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Registered trials
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