Alzheimer's disease (AD) is a highly debilitating neurodegenerative disorder
characterized by cognitive dysfunction, inflammation and oxidative stress are thought
to play major roles in pathophysiology of the AD, which of them have a principle role
is unclear. The role of brain growth factors, cytokines and oxidative biomarkers in
cognitive dysfunction induced by AlCL3 in rats with application of anti-inflammatory
(cilostazol) and antioxidant (N-acetyl cysteine, NAC) were investigated to clarify the
predominant pathophysiological mechanism involved. Methods: Alzheimer's model
group was given AlCL3 (100 mg/kg-) orally for 6 weeks. Alzheimer's model + NAC
and Alzheimer's model + cilostazol groups were given (NAC) and cilostazol
respectively one hr. before AlCL3 for the same duration. Results: anti-inflammatory
or antioxidant significantly improved memory retention which was evaluated by
Morris Water Maze, passive avoidance task and eight-arm radial maze. This
improvement was consistent with histological recovery and was mediated by
reduction AlCL3 concentration in the brain hippocampus and frontal cortex,
interference with the cholinergic dysfunction as well as prevention of oxidative
damage. In addition, anti-inflammatory agent can modulate superiorly the
inflammatory response via reduction the levels of inflammatory cytokines and
adjustment the levels of brain–derived neurotrophic factors and transforming growth
factor B. This finding supports the principal role of inflammation in pathophysiology
of AD and suggests the potential therapeutic application of anti-inflammatory agent
for this condition.