Abstract: Objective: This study aimed to explore the effects and potential mechanisms of WGX-50 (N-2-(3,4-dimethoxyphenyl)ethyl-3-phenyl-acrylamide) in mitigating the progression of early Alzheimer's disease (AD). Methods: Network pharmacology and molecular docking simulations were employed to identify key targets of WGX-50 in AD intervention. A 60-day intervention was conducted in 12-week-old 3xTg-AD mouse models via intraperitoneal injection of 1 mg/kg/day WGX-50. The improved effects of WGX-50 intervention on cognitive function in AD mice were evaluated through the water maze test and open field test. To explore the potential mechanism of WGX-50 in AD intervention, various methods were used to detect and evaluate key indicators. ELISA was used to detect serum inflammatory markers level. The hippocampal histological features were observed by HE and Nissl staining. Fecal metabolomic profiles were preliminarily analyzed by untargeted metabolomics. Glucose tolerance in mice was evaluated via glucose tolerance test. Results: The key targets of WGX-50 intervention on AD were primarily enriched in the TNF signaling pathway, PI3K-Akt signaling pathway, and MAPK signaling pathway. The WGX-50 intervention resulted in significant enhancements in glucose tolerance and behavioural performance (learning, memory, and spontaneous activity). Concurrently, attenuated neuronal damage in the hippocampus and a decrease in the level of pro-inflammatory factors (IL-6, IL-1β, TNF-α, IL-8), inflammatory markers (C-reactive protein), and inflammatory injury markers (MPO), as well as reduced expression of protein kinase B1 (AKT1)(P<0.05), were also observed. Among the 30 fecal differential metabolites identified, 10 were upregulated and 20 were downregulated. Five major pathways were identified through intergroup comparisons(P<0.05), including Primary bile acid biosynthesis and tryptophan metabolism. Conclusions: WGX-50 inhibited neuroinflammation mediated by TNF signaling pathway, PI3K-Akt signaling pathway, primary bile acid biosynthesis, tryptophan metabolism, and other pathways to delay early AD progression and improve cognitive function.