Abstract
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.
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.
| Originalsprache | Englisch |
|---|---|
| Zeitschrift | research square |
| Seitenumfang | 26 |
| DOIs | |
| Publikationsstatus | Veröffentlicht - 2021 |
Strategische Forschungsbereiche und Zentren
- Forschungsschwerpunkt: Gehirn, Hormone, Verhalten - Center for Brain, Behavior and Metabolism (CBBM)
UN SDGs
Dieser Output leistet einen Beitrag zu folgendem(n) Ziel(en) für nachhaltige Entwicklung
