Abstract
Abstract
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 efect of policosanol (PCO) on
cognitive function, oxidative-antioxidative status, and amyloid-beta (Aβ) plaque formation in an AD rat model induced
by intracerebroventricular (ICV) injection of Aβ1–40. Healthy adult male Wistar rats were randomly divided into seven
groups: control, sham (5 μL, ICV injection of phosphate-bufered saline), 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). 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 Aβ plaques were detected by Congo red staining. The results showed that injection of Aβ 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 Aβ resulted in increased
total oxidant status, decreased total antioxidant capacity, and enhanced Aβ plaque formation in the rats. Intriguingly, PCO
treatment improved all the above-mentioned neuropathological changes in the Aβ-induced AD rats. The results suggest that
PCO improves Aβ-induced cognitive decline, possibly through modulation of oxidative-antioxidative status and inhibition
of Aβ plaque formation.
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 efect of policosanol (PCO) on
cognitive function, oxidative-antioxidative status, and amyloid-beta (Aβ) plaque formation in an AD rat model induced
by intracerebroventricular (ICV) injection of Aβ1–40. Healthy adult male Wistar rats were randomly divided into seven
groups: control, sham (5 μL, ICV injection of phosphate-bufered saline), 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). 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 Aβ plaques were detected by Congo red staining. The results showed that injection of Aβ 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 Aβ resulted in increased
total oxidant status, decreased total antioxidant capacity, and enhanced Aβ plaque formation in the rats. Intriguingly, PCO
treatment improved all the above-mentioned neuropathological changes in the Aβ-induced AD rats. The results suggest that
PCO improves Aβ-induced cognitive decline, possibly through modulation of oxidative-antioxidative status and inhibition
of Aβ plaque formation.
| Original language | English |
|---|---|
| Journal | Molecular Neurobiology |
| Volume | 60 |
| Issue number | 5 |
| Pages (from-to) | 2507-2519 |
| Number of pages | 13 |
| ISSN | 0893-7648 |
| DOIs | |
| Publication status | Published - 05.2023 |
Research Areas and Centers
- Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)
DFG Research Classification Scheme
- 205-09 Pharmacology
