نیلوفر دربندی

Background and purpose: Alzheimer's disease is a neurodegenerative disorder associated with the accumulation of amyloid plaques in neurons. Increase in blood cholesterol leads to an increase in the deposition of these proteins in neurons and results in memory degradation. In the present study, the effect of rosuvastatin as a cholesterol-lowering drug was investigated in Alzheimer's rats. Materials and methods: Animals were divided into four groups: control, streptozotocin (to induce Alzheimer's), rosuvastatin, and rosuvastatin with streptozotocin. In intracerebroventricular injection, the groups received saline (1 μg/mouse) or streptozotocin (3 mg/kg). Daily gavage of saline (1 mg/kg) or rosuvastatin (10, 20 mg/kg) started one day before cannulation and continued for two weeks. At the end of the treatment period, the rats' memory, number of healthy neurons in CA1 area, and serum oxidative stress indices were measured. Results: Intraventricular injection of streptozotocin significantly decreased memory recall, the number of intact neurons in CA1 area, total antioxidant power, and superoxide dismutase enzyme level; and increased serum malondialdehyde levels compared to the control group (P<0.001). In the group receiving rosuvastatin (20 mg/kg), the above indexes were significantly reversed compared to the streptozotocin group (P<0.001), which means improved memory. In rosuvastatin groups (10 and 20 mg/kg) alone, there was no significant difference in the above indexes compared to the control group (P>0.05). Conclusion: Streptozotocin leads to cell death in the CA1 region and memory dysfunction through various mechanisms such as increasing oxidative stress. It seems that rosuvastatin is able to prevent the destructive effects of streptozotocin on memory and learning by inhibiting oxidative stress indicators.