A 4.7-kDa polysaccharide from Panax ginseng suppresses Aß pathology via mitophagy activation in cross-species Alzheimer's disease models.
Biomed Pharmacother
; 167: 115442, 2023 Nov.
Article
in En
| MEDLINE
| ID: mdl-37699318
Alzheimer's disease (AD) is a neurological condition that progresses with age. Amyloid-ß (Aß) aggregation has been suggested to be a key pathogenic process in Alzheimer's disease. Ginseng polysaccharides (GP), the main biologically active components isolated from Panax ginseng C. A. Meyer (ginseng), may act as neuroprotective agents with potential benefits for AD patients. However, GP effects on Aß pathology and AD symptoms are still unclear. Here, a 4.7-kDa GP termed GP4 was purified and subjected to basic physicochemical characterization. The biological effects of GP4 to prevent Aß aggregation were then assessed with cross-species AD models, including Aftin-5-treated SH-SY5Y cells and cerebral organoids, and transgenic C. elegans overexpressing the full-length human Aß42 peptide. These analyses ultimately demonstrated that GP4 was capable of inhibiting Aß accumulation both in vivo and vitro, and with early intervention of GP4 being sufficient to alleviate Aß42-associated aging phenotypes and memory loss in C. elegans model of AD. Furthermore, neuroinflammation was significantly down-regulated in human cells and cerebral organoids. From a mechanistic perspective, the ability of GP4 to inhibit Aß aggregation was found to be related to its ability to promote neuronal mitophagic activity. This finding offers a robust theoretical foundation for the further development of GP4 as a candidate drugs with the potential to treat AD.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Type of study:
Prognostic_studies
Language:
En
Journal:
Biomed Pharmacother
Year:
2023
Document type:
Article
Affiliation country:
China
Country of publication:
France