Alzheimer's disease (AD) is the most prevalent neurodegenerative disease in the world. However, there is no effective drug to cure it. Caesalmin C is a cassane-type diterpenoid abundant in (Linn.) Roxb. In this study, we investigated the effect of caesalmin C on Aβ-induced toxicity and possible mechanisms in the transgenic AD model. Our results showed that caesalmin C significantly alleviated the Aβ-induced paralysis phenotype in transgenic CL4176 strain . Caesalmin C dramatically reduced the content of Aβ monomers, oligomers, and deposited spots in AD . In addition, mRNA levels of , , and were up-regulated, and mRNA levels of were down-regulated in nematodes treated with caesalmin C. The results of the RNAi assay showed that the inhibitory effect of caesalmin C on the nematode paralysis phenotype required the DAF-16 signaling pathway, but not SKN-1 and HSF-1. Further evidence suggested that caesalmin C may also have the effect of inhibiting acetylcholinesterase (AchE) and upregulating proteasome activity. These findings suggest that caesalmin C delays the progression of AD in via the DAF-16 signaling pathway and that it could be developed into a promising medication to treat AD.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9225120 | PMC |
http://dx.doi.org/10.3390/ijms23126871 | DOI Listing |
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