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Alzheimer's disease (AD) is a neurodegenerative disease clinically characterized by progressive cognitive impairment. This work aimed to investigate the role of quercetin (Q) in the treatment and protection of AlCl3-induced AD in rats through exploring the molecular mechanisms underlying its neuroprotective and therapeutic properties. In this study, male Wistar rats were allocated to two experiments: experiment I (therapeutic effect of quercetin) in which the rats were divided into: normal control group (C-Saline) which was induced with saline for 56 days, C-Q50 group, which was administered orally with Q (50 mg/kg) for 28 days after induction saline for 28 days, AD (AlCl3-Saline) group received AlCl3 (50 mg/kg) intraperitoneally for 28 days followed by saline for 28 days, and the AlCl3-Q50 group received Q (50 mg/kg) orally for 28 days after induction with AlCl3 for 28 days. In experiment II rats were divided into: normal control (NC) group, Q50 (50 mg/ kg) group, AlCl3 (AD) group, and AlCl3 + Q50 group which was co-administrated with AlCl3 + Q50 for 56 successive days. Dopamine (DA) and acetylcholinesterase) AChE (levels were estimated for all rat groups. The results showed that post-treatment of the AD-induced rats with Q50 as well as co-administration of AlCl3with Q50, significantly reduced the AChE level in serum, significantly increased the DA level, and significantly increased the body weight change compared to the AlCl3group, but did not show any significant change in the brain weight. We concluded that quercetin significantly improved the cholinergic and dopaminergic dysfunctions by lowering the Acetylcholine esterase level and restoring the dopamine level |
