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<p>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 <i>Caenorhabditis elegans</i>. SumI activated the HLH-30 transcription factor by triggering a lipid-catabolic response akin to starvation. <i>bec-1</i> RNAi significantly abrogated the anti-AD effect of SumI. Our findings indicate that SumI mitigated protein aggregation by activating the autophagy-lysosome pathway in <i>C. elegans</i> and provide scientific evidence that ginsenoside composition could be a potential therapeutic agent for treating or preventing AD.</p> Graphical abstract <p></p>

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A Ginsenoside Composition Ameliorated Aβ and Tau Aggregation via Autophagy Lysosome Pathway

  • 期刊论文

  • 发表日期：

    2025年5月6日

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  • Chengmu Zhao,
  • Juan Yue,
  • Yu Xie,
  • Bo Liu,
  • Shuaishuai Xu,
  • Dejuan Zhi,
  • Dongsheng Wang

摘要

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.

Graphical abstract