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Year : 2014  |  Volume : 6  |  Issue : 3  |  Page : 130-144

Inflammation versus oxidative stress in pathophysiology of alzheimer's disease in rat model

1 Department of Physiology, Faculty of Medicine, Assiut Univerisity, Assiut, Egypt
2 Department of Forensic & Clinical Toxicology, Faculty of Medicine, Assiut University, Assiut, Egypt

Correspondence Address:
Omyma Galal Ahmed
Department of Physiology, Faculty of Medicine, Assiut Univerisity, Assiut
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1947-489X.210374

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Background: 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 the pathophysiology. Which one has the principle role is unclear. Objectives: The role of brain growth factors, cytokines and oxidative biomarkers in cognitive dysfunction induced by Aluminium chloride (AlCl3) in rats with application of an anti-inflammatory (Cilostazol) and an 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 six weeks. Alzheimer's model + NAC, and Alzheimer's model + Cilostazol groups were given (NAC) and Cilostazol respectively one hour before AlCl3 for the same duration. Results: Anti-inflammatory or antioxidant interventions 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 agents can modulate superiorly the inflammatory response via reduction of the levels of inflammatory cytokines and adjustment of the levels of brain–derived neurotrophic factors and transforming growth factor B. Conclusions: These finding support the principal role of inflammation in pathophysiology of AD and suggests the potential therapeutic application of anti-inflammatory agents for this condition.

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