Neuroprotective effect of quercetin through targeting key genes involved in aluminum chloride induced Alzheimer’s disease in rats
Hala Elreedy, Asmaa M. Elfiky, Asmaa Mahmoud, Khadiga S. Ibrahim, Mohamed A. Ghazy
Abstract
Alzheimer’s disease (AD) is a neurodegenerative disorder that is clinically characterized by deteriorating cognitive function. Quercetin (Q), a bioflavonoid, has been reported to slow down AD progression. Q at a dose of 50 mg/kg-1 shows an important therapeutic effect in aluminum chloride (AlCl3)-induced Alzheimer’s disease, which has been previously published by us. Here, this study aimed to highlight the neuroprotective effect of quercetin on hallmark genes in AlCl3-induced Alzheimer’s disease in rats. Wistar male rats were subjected to a vehicle group, AlCl3 group, and co-administration with AlCl3 + Q50 for 60 sequential days. Behavioral tests and qPCR were performed to assess the efficacy of Q. The co-administration of quercetin (50 mg kg-1) has a significant effect on memory deficits. Furthermore, AlCl3 + Q50 group resulted in significantly decreased amyloid precursor protein levels (APP), β-amyloid converting enzyme 1 (BACE1), and presenilin I (PSEN1) and increased the expression of ADAM17 in the hippocampus tissue compared to AlCl3 group (p < 0.05). The current study showed that the quercetin’s neuroprotective properties may involve its ability to target the most significant Alzheimer’s disease-related genes and slow the progression of cognitive impairment.