Harnessing the power of ginger leaf polysaccharide: A potential strategy to combat Aβ-induced toxicity through the Wnt/β-catenin pathway

Alzheimer's disease (AD) is prevalent in the elderly, with amyloid-β (Aβ) playing a critical role in its progression. Polysaccharides have garnered increasing attention due to their low toxicity and diverse applications in alleviating AD-like symptoms. However, the potential of ginger leaf polysaccharide in mitigating AD-like symptoms has been rarely investigated. In this study, we isolated a polysaccharide (GLP1) from ginger leaf and evaluated its efficacy and underlying mechanisms in alleviating AD-like symptoms using Caenorhabditis elegans and PC12 cells. GLP1 ameliorated AD-like symptoms in C. elegans , as evidenced by a 41.50 % increase in head thrashing frequency and an 87.13 % increase in body bending frequency. Furthermore, GLP1 mitigated cognitive decline by 76.51 %. Additionally, GLP1 enhanced the activity of acetylcholinesterase in C. elegans and maintained the integrity of neural system function. Moreover, GLP1 improved the survival rate of PC12 cells under Aβ induction by activating the Wnt/β-catenin pathway, which also resulted in a reduction in the release of inflammatory factors, specifically IL-1β by 21.15 %, IL-6 by 39.98 %, and TNF-α by 19.66 %. Notably, FITC-labeled GLP1 could be absorbed by PC12 cells. These compelling findings underscored the therapeutic potential of GLP1 in alleviating Aβ-induced AD-like symptoms and supported the advancement of ginger leaf resource utilization.