Hippocampal beta-amyloid accumulation in aluminium chloride and D-galactose-induced rats: establishing a nontransgenic Alzheimer’s model

Alzheimer’s disease (AD) is characterized by tau protein aggregation and beta-amyloid (Aβ) plaques leading to progressive cognitive decline. Nontransgenic models using aluminium chloride (AlCl 3)and D-galactose (D-gal) have been established to mimic AD pathology, but beta-amyloid deposition in hippocampal regions remains underexplored. Objective: To investigate beta-amyloid accumulation in the hippocampal CA2 region using a nontransgenic rat model of AD made by combined AlCl 3 and D-gal administration. Methods: Twelve adults male Wistar rats were divided into control ( n = 6) and model groups ( n = 6). The control group received normal saline orally and water intraperitoneally. The model group received D-gal (60 mg/kg b.w., i.p.) and AlCl 3 (200 mg/kg b.w., oral) daily for 10 weeks. Beta-amyloid expression in hippocampal CA2 region was assessed using immunohistochemistry. Results: Immunohistochemical analysis revealed marked beta-amyloid immunoreactivity in the model group, with dense extracellular and intracellular deposits distributed throughout the CA2 subfield. The control group showed minimal beta-amyloid staining without plaques, confirming the specificity of the observed pathology. Conclusion: Combined AlCl 3 and D-gal administration successfully induced significant beta-amyloid accumulation in the hippocampal CA2 region, validating this nontransgenic model for investigating AD pathogenesis. This model provides a valuable platform for studying sporadic AD mechanisms and evaluating potential therapeutic interventions.

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