Comparison and Exploration of Aluminum Toxicity and β-Amyloid Protein Theories

This study explored the link between aluminum (Al) toxicity and beta-amyloid pathology in 52 SPF mice divided into control (saline), low- (2 mg/kg), medium- (4 mg/kg), and high-dose (8 mg/kg) maltol aluminum groups. After 60 days of intraperitoneal injections, Y-maze tests revealed significant learning and memory impairments in medium/high-dose groups (P<0.05). Serum analysis showed elevated TC, TP, and ALT but reduced BUN and Hb in Al-exposed groups (P<0.05). Brain tissue analysis indicated higher Al³⁺ levels in all treated groups (P<0.05), with reduced acetylcholinesterase (AchE) activity in medium/high doses (P<0.05). BACE1 protein (a key enzyme in amyloid production) increased significantly in the high-dose group (P<0.05). Glutathione peroxidase (GSH-PX) levels varied, with serum GSH-PX elevated in the medium-dose group (P<0.05) but brain GSH-PX reduced in medium and elevated in high doses (P<0.05). Aluminum exposure may promote beta-amyloid generation via BACE1 upregulation, impairing cognitive function, supporting a potential mechanistic link between Al toxicity and Alzheimer's-like pathology.