Protective effects of selegiline against amyloid beta‐induced anxiety‐like behavior and memory impairment

Background Alzheimer's disease (AD) is a complex and common neurodegenerative disorder. The present study aimed to investigate the potential effects of selegiline (SEL) on various aspects of memory performance, anxiety, and oxidative stress in an AD rat model induced by intracerebroventricular...

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Veröffentlicht in:Brain and behavior 2024-06, Vol.14 (6), p.e3599-n/a
Hauptverfasser: Mohamadpour, Behnam, Mirazi, Naser, Komaki, Alireza, Basir, Hamid Shokati, Hosseini, Abdolkarim
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Sprache:eng
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Zusammenfassung:Background Alzheimer's disease (AD) is a complex and common neurodegenerative disorder. The present study aimed to investigate the potential effects of selegiline (SEL) on various aspects of memory performance, anxiety, and oxidative stress in an AD rat model induced by intracerebroventricular injection of amyloid beta1‐42 (Aβ1‐42). Methods Oral administration of SEL at a dose of 0.5 mg/kg/day was performed for 30 consecutive days. Following the 30 days, several tests, including the open‐field, elevated plus‐maze, novel object recognition, Morris water maze, and passive avoidance learning were conducted to assess locomotor activity, anxiety‐like behavior, recognition memory, spatial memory, and passive avoidance memory, respectively. Results The results indicate that the induction of AD in rats led to recognition memory, spatial memory, and passive avoidance memory impairments, as well as increased anxiety. Additionally, the AD rats exhibited a decrease in total antioxidant capacity and an increase in total oxidant status levels, suggesting an imbalance in oxidative‐antioxidant status. However, the administration of SEL improved memory performance, reduced anxiety, and modulated oxidative‐antioxidant status in AD rats. Conclusions These findings provide evidence that SEL may alleviate anxiety‐like behavior and cognitive deficits induced by Aβ through modulation of oxidative‐antioxidant status.
ISSN:2162-3279
2162-3279
DOI:10.1002/brb3.3599