Study on the Effects of Subchronic Aluminum Exposure on the Activities of Brain α-Secretase and γ-Secretase in Alzheimer's Disease Model Mice

This study explored the impact of subchronic aluminum exposure on brain α-secretase and γ-secretase activities in AD model mice. Thirty Kunming mice were randomized into a normal group, a low-dose group (0.3 mL of 50 mg/kg aluminum maltolate, i.p.), and a high-dose group (0.45 mL of 75 mg/kg aluminum maltolate, i.p.), with daily treatments for 30 days. Spatial memory was assessed using the Y-maze water labyrinth^[1]. Brain homogenate enzyme activities and serum biochemical markers (urea nitrogen, TC, TG) were measured via standard protocols. Results showed increased aluminum exposure significantly prolonged swimming latency and path length in the water labyrinth (P < 0.05, one-way ANOVA), coupled with reduced α/γ-secretase activities compared to the normal group. Aluminum maltolate (Al(mal)₃) exposure induced AD-like symptoms, including cognitive dysfunction and neuronal damage, as reflected by impaired spatial learning in the Y-maze^[2].In conclusion, subchronic aluminum exposure contributes to AD pathogenesis by dysregulating α/γ-secretase, influencing Aβ metabolism. These findings provide experimental basis for preventing aluminum-related neurodegenerative diseases.