Neuroprotective effect of quercetin through targeting key genes involved in aluminum chloride induced Alzheimer’s disease in rats

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.