| Abstrakt: |
Introduction: Alzheimer’s disease (AD), one of the leading causes of dementia, is characterized by progressive loss of cognitive performance and synaptic plasticity. The present study was designed to examine the putative effects of selegiline on passive avoidance memory function and to identify the roles of hippocampal synaptic plasticity and oxidative stress in an AD rat model induced by intracerebroventricular (ICV) injection of Aβ. Methods and Materials: LTP induction and passive avoidance memory were assessed in selegiline-treated rats (5 mg/kg/day). Moreover, serum levels of oxidative stress biomarkers, total thiol group (TTG) and malondialdehyde (MDA), and deposition of Aβ plaques in rat’s brains were evaluated. Results: The results showed that AD-induced Aβ impaired passive avoidance memory, which was paralleled by a reduction in fEPSPs slope, PS amplitude, and TTG content, and an increase in MDA level and Aβ plaque formation in the rats. In contrast, selegiline treatment ameliorated passive avoidance memory dysfunction improved hippocampal LTP impairment, modulated oxidative-antioxidative status, and hindered Aβ plaques production in AD rats. Conclusion: This data provides evidence that selegiline alleviates Aβ-induced cognitive deficit, probably by amelioration of hippocampal LTP impairment, modulation of oxidative-antioxidative status, and inhibition of Aβ plaque accumulation. [ABSTRACT FROM AUTHOR] |
