Abstract
Abstract
Rationale Alzheimer’s disease (AD) is a chronic neurodegenerative disorder characterized by cognitive decline and synaptic
failure.
Objective The present study was designed to explore the possible protective efects of policosanol (PCO) on spatial cognitive
capacity, long-term potentiation (LTP) induction, oxidant/antioxidant status, and Aβ plaques formation in an AD rat model
induced by intracerebroventricular (ICV) injection of Aβ1–40.
Methods Healthy adult male Wistar rats were randomly divided into control, sham (ICV injection of 5 µl phosphate-bufered
saline), AG (50 mg/kg; P.O., as PCO vehicle), PCO (50 mg/kg; P.O.), AD model (ICV injection of 5 µl Aβ), AD+AG (50 mg/
kg; P.O.), and AD+PCO (50 mg/kg; P.O.). Treatments were performed for eight consecutive weeks. At the end of the treatment course, spatial learning and memory functions, hippocampal long-term potentiation (LTP) induction, malondialdehyde
(MDA), and total thiol group (TTG) levels, as well as the formation of Aβ plaques, were examined.
Results The results showed that injection of Aβ reduced spatial learning and memory abilities in the Barnes maze test, which
was accompanied by decreases in feld excitatory postsynaptic potential (fEPSP) slope, population spike (PS) amplitude,
and TTG level and increases in Aβ plaque accumulation and MDA content. In contrast, PCO treatment improved all the
above-mentioned changes in the Aβ-infused rats.
Conclusions The results suggest that amelioration of hippocampal synaptic plasticity impairment, modulation of oxidant/
antioxidant status, and inhibition of Aβ plaque formation by PCO may be the mechanisms behind its protective efect against
AD-associated spatial cognitive decline
Rationale Alzheimer’s disease (AD) is a chronic neurodegenerative disorder characterized by cognitive decline and synaptic
failure.
Objective The present study was designed to explore the possible protective efects of policosanol (PCO) on spatial cognitive
capacity, long-term potentiation (LTP) induction, oxidant/antioxidant status, and Aβ plaques formation in an AD rat model
induced by intracerebroventricular (ICV) injection of Aβ1–40.
Methods Healthy adult male Wistar rats were randomly divided into control, sham (ICV injection of 5 µl phosphate-bufered
saline), AG (50 mg/kg; P.O., as PCO vehicle), PCO (50 mg/kg; P.O.), AD model (ICV injection of 5 µl Aβ), AD+AG (50 mg/
kg; P.O.), and AD+PCO (50 mg/kg; P.O.). Treatments were performed for eight consecutive weeks. At the end of the treatment course, spatial learning and memory functions, hippocampal long-term potentiation (LTP) induction, malondialdehyde
(MDA), and total thiol group (TTG) levels, as well as the formation of Aβ plaques, were examined.
Results The results showed that injection of Aβ reduced spatial learning and memory abilities in the Barnes maze test, which
was accompanied by decreases in feld excitatory postsynaptic potential (fEPSP) slope, population spike (PS) amplitude,
and TTG level and increases in Aβ plaque accumulation and MDA content. In contrast, PCO treatment improved all the
above-mentioned changes in the Aβ-infused rats.
Conclusions The results suggest that amelioration of hippocampal synaptic plasticity impairment, modulation of oxidant/
antioxidant status, and inhibition of Aβ plaque formation by PCO may be the mechanisms behind its protective efect against
AD-associated spatial cognitive decline
| Original language | English |
|---|---|
| Journal | Psychopharmacology |
| Volume | 240 |
| Issue number | 4 |
| Pages (from-to) | 755-767 |
| Number of pages | 13 |
| ISSN | 0033-3158 |
| DOIs | |
| Publication status | Published - 04.2023 |
Research Areas and Centers
- Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)
DFG Research Classification Scheme
- 2.22-09 Pharmacology
