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

Alzheimer's disease (AD), the most common form of dementia, is characterized by a progressive decline in cognitive performance and memory formation. The present study was designed to investigate the effect of policosanol (PCO) on cognitive function, oxidative-antioxidative status, and amyloid-beta (A beta) plaque formation in an AD rat model induced by intracerebroventricular (ICV) injection of A beta(1-40). Healthy adult male Wistar rats were randomly divided into seven groups: control, sham (5 mu L, ICV injection of phosphate-buffered saline), AD model (5 mu L, ICV injection of A beta), 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). During the ninth and tenth weeks of the study, the cognitive function of the rats was assessed by commonly used behavioral paradigms. Subsequently, oxidative-antioxidative status was examined in the serum. Moreover, compact A beta plaques were detected by Congo red staining. The results showed that injection of A beta impaired recognition memory in the novel object recognition test, reduced the spatial cognitive ability in the Morris water maze, and alleviated retention and recall capability in the passive avoidance task. Additionally, injection of A beta resulted in increased total oxidant status, decreased total antioxidant capacity, and enhanced A beta plaque formation in the rats. Intriguingly, PCO treatment improved all the above-mentioned neuropathological changes in the A beta-induced AD rats. The results suggest that PCO improves A beta-induced cognitive decline, possibly through modulation of oxidative-antioxidative status and inhibition of A beta plaque formation.