Akademik Veri Yönetim Sistemi
ARS PHARMACEUTICA, cilt.67, sa.3, ss.354-363, 2026 (ESCI)
Introduction: Aluminium is a ubiquitous neurotoxin associated with Alzheimer’s disease pathology. In this study, we aimed to investigate the effects of subchronic oral aluminium administration on spatial memory and neuroin flammatory markers, as well as the potential impact of concurrent metformin administration on these changes. Method: Wistar albino rats were divided into six groups: Control, Al (70 mg/kg via drinking water), Metformin (100 and 200 mg/kg i.p.), and Al + Metformin 100 and 200 mg/kg for 49 days. Spatial learning and memory were assessed using the Morris Water Maze, while locomotor activity was evaluated via Open Field tests. Hippocampal tissues were analysed for amyloid-β plaques, morphology, and inflammatory markers (TNF-α, IL-1β, IL-6, IL-8, Amyloid-β1-42) via ELISA and histology. Results: Results indicated no significant deficits in spatial memory or locomotor activity among groups. Histo pathological examination revealed no amyloid deposition or significant morphological changes. Molecular analysis showed no consistent alteration in inflammatory markers, except for an isolated increase in IL-1β in the high-dose metformin co-treated group. Conclusions: The oral administration of 70 mg/kg Aluminum for 49 days did not elicit detectable neurotoxicity, likely due to limited gastrointestinal absorption; consequently, the neuroprotective potential of metformin could not be effectively evaluated. These findings suggest that subchronic oral Al exposure via drinking water may be an insensitive model for inducing Alzheimer’s Disease-like pathology in rats, highlighting the necessity for alternative administration routes or extended exposure durations in future toxicological assessments