The Neuroprotective Effects of Policosanol on Learning and Memory Impairment in a Male Rat Model of Alzheimer's Disease

Alzheimer's disease (AD) as a neurodegenerative disease is recognized with progressive cognitive function failure, which is determined by beta-amyloid (Aβ) accumulation in extracellular space and hyperphosphorylation of intracellular Tau protein. Aβ stimulates some kinds of active oxygen and causes oxidative stresses and apoptosis. Policosanol (PCO) is a reducing lipid complement, which has antioxidant and anti-inflammatory activities. In the current research, the PCO effects on learning and memory impairment were investigated in a rat model of AD. Healthy adult male Wistar rats (230–250g) were divided randomly into 7 groups (n=6-7): Control, Sham (5 µL of phosphate-buffered saline, intracerebroventricular (ICV) microinjection), AD model (5 µL, ICV injection of Aβ), acacia gum (50 mg/kg, 8 weeks, gavage), PCO (50 mg/kg, 8 weeks, gavage), AD + acacia gum (50 mg/kg, 8 weeks, gavage), and AD + PCO (50 mg/kg, 8 weeks, gavage). Passive avoidance learning (PAL) and memory were assessed by shuttle box, cognitive memory by novel object recognition (NOR), and spatial memory by the Morris water maze (MWM) test. The oxidant and antioxidant parameters were examined at the end of the experiments. According to our results, ICV injection of Aβ caused reduced cognitive memory in NOR, spatial memory in MWM, and passive avoidance in PAL tests. PCO caused a recovery in cognitive memory, spatial memory, and PAL memory. Aβ plaques increased in the AD group, while PCO decreased it. Aβ increased total oxidant status and decreased total antioxidant capacity, whereas PCO reversed these parameters. Our results demonstrated that PCO has neuroprotective effects and can protect learning and memory impairments via its hypolipidemic and antioxidant effects.