فهرست نشریات علمی دسترسی آزاد ایران

Alzheimer’s disease is characterized by cognitive decline and neuroinflammation caused by the accumulation of amyloid-β plaques and neurofibrillary tangles. While environmental aluminum exposure has been suggested as a possible cause of AD-like conditions, its specific impact on behavioral domains and inflammatory metabolic pathways remain unclear. Adult wild-type zebrafish (5-6 months old) were exposed to three different concentrations of aluminum chloride (AlCl₃, doses of 200, 350, and 500 µg/L) for 28 days. Behavioral impairment was assessed via the novel tank diving test (NTDT), open field test (OFT), Shoaling Test, and Novel Object Recognition Test (NORT). Molecular changes in appb, mapt, and ido1 gene expressions were quantified using quantitative real-time PCR (qRT-PCR). AlCl₃ exposure induced dose-dependent behavioral alterations. The 350 µg/L group exhibited the most noticeable behavioral disruption, including increased anxiety-like behavior, reduced shoaling cohesiveness, and impaired recognition memory. In contrast, the 500 µg/L group exhibited behavioral adaptation in locomotion. Molecular analysis revealed significant upregulation of appb and mapt, along with a marked increase in ido1 gene expression at 500 µg/L, indicating activation of the tryptophan-kynurenine pathway. Chronic AlCl₃ exposure in zebrafish reproduces several behavioral and biochemical features associated with early-stage AD. These findings suggest that ido1-mediated tryptophan metabolism and neuroinflammation are critical links between aluminum toxicity and functional cognitive decline.