The effect of the flavonoid quercetin on the modulation of the amyloid pathway in Aluminum chloride-induced Alzheimer disease in rats

Abstract

Alzheimer’s disease (AD) is a complex progressive neurodegenerative and dementing disorder that is only clinically diagnosed at the end stage. AD is a leading cause of dementia, causing progressive loss of memory and cognition and affecting 46.8 million people globally. The hallmarks of this disorder are the extracellular aggregation of amyloid β (Aβ) peptides (Aβ plaques) in senile plaques (SP) and the intracellular deposition of hyperphosphorylated tau protein (NFT) in the hippocampus and neocortex . Many risk factors have been associated with AD including those related to aging, genes, metals, traumatic brain injury, diet, vascular factors, the immune system, and exposure to infectious agents. Aluminum is a widespread chronic neurotoxin thus exposure to aluminum chloride leads to the accumulation of intermediary toxic compounds such as hydrogen peroxide and hydroxyl radicals, which may mediate the toxicity of aluminum. Also the activities of antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase are decreased, whereas xanthine oxidase is increased following exposure to aluminum chloride .It is stated that aluminum, a well-established neurotoxicant, owing to its simple entry and retention in the central nervous system, is implicated in the etiology of (AD). Quercetin is one of the most potent plant origin antioxidants and is one of the most prevalent flavonoids found in edible plants. Numerous biochemical and pharmacological activities, such as free-radical scavenging, have been reported to Q as well as it affects the immune and inflammatory