Abstract
Alzheimer’s disease (AD) is a neurodegenerative disease with cognitive impairment. Oxidative stress in neurons is considered as a reason for development of AD. Antioxidant agents such as quercetin slow down AD progression, but the usage of this flavonoid has limitations because of its low bioavailability. We hypothesized that quercetin-conjugated superparamagnetic iron oxide nanoparticles (QT-SPIONs) have a better neuroprotective effect on AD than free quercetin and regulates the antioxidant, apoptotic, and APP gene, and miRNA-101. In this study, male Wistar rats were subjected to AlCl3, AlCl3 + QT, AlCl3 + SPION, and AlCl3 + QT-SPION for 42 consecutive days. Behavioral tests and qPCR were used to evaluate the efficiency of treatments. Results of behavioral tests revealed that the intensity of cognitive impairment was decelerated at both the middle and end of the treatment period. The effect of QT-SPIONs on learning and memory deficits were closely similar to the control group. The increase in expression levels of APP gene and the decrease in mir101 led to the development of AD symptoms in rats treated with AlCl3 while these results were reversed in the AlCl3 + QT-SPIONs group. This group showed similar results with the control group. QT-SPION also decreased the expression levels of antioxidant enzymes along with increases in expression levels of anti-apoptotic genes. Accordingly, the antioxidant effect of QT-SPION inhibited progression of cognitive impairment via sustaining the balance of antioxidant enzymes in the hippocampus of AD model rats.
Highlights
Alzheimer’s disease (AD) appears as an outcome of neurodegeneration that is recognized with symptoms of intensive cognitive impairment (Ramalho et al, 2020)
QRT-PCR results revealed that expression levels of BCL2 as an antiapoptotic gene showed a significant decrease in the AlCl3 group compared to the control group (p < 0.001); simultaneous treatment of AlCl3 and QT-SPION in the AlCl3 + QT-SPION group led to a recovery effect against the destructive effect of AlCl3 compared to the AlCl3 group (Figure 7F)
Results of quantitative real-time PCR (qRT-PCR) for BAX as a proapoptotic gene showed significantly higher expression levels in the AlCl3 group compared to the control group (p < 0.001), while this effect was recovered in the AlCl3 + QT-SPION group via treatment with QT-SPION, and these results were similar to the control group (Figure 7H)
Summary
Alzheimer’s disease (AD) appears as an outcome of neurodegeneration that is recognized with symptoms of intensive cognitive impairment (Ramalho et al, 2020). AD appears in people older than 60 years old (Santamaría et al, 2020). The main AD symptoms include Aβ decomposition and tau hyperphosphorylation (Madav et al, 2019; Zaplatic et al, 2019). During the AD progression, mitochondria impairment leads to increased production of ROS, which, in turn, is the cause of decreased levels of antioxidant enzymes and can result in neural cell death
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