article · Egyptian Journal of Basic and Applied Sciences
Alzheimer's disease is a neurodegenerative condition marked by worsening cognitive decline. Research evaluated the neuroprotective effects of the bioflavonoid quercetin on hallmark genes associated with Alzheimer's disease using a rat model. Male Wistar rats were treated over 60 consecutive days with aluminum chloride alone, a control vehicle, or aluminum chloride combined with quercetin at a dose of 50 mg/kg. Evaluation through behavioural testing demonstrated that co-administering quercetin significantly improved memory deficits. Furthermore, quantitative real-time PCR showed that quercetin treatment decreased hippocampal levels of amyloid precursor protein, beta-amyloid converting enzyme 1, and presenilin 1, while elevating ADAM17 expression compared to the aluminum chloride group. These results indicate that quercetin exerts protective effects in the brain by modulating key disease-related genes and reducing the rate of cognitive deterioration.
Alzheimer's disease causes severe cognitive decline with few effective long-term solutions. Demonstrating that a dietary bioflavonoid can regulate key genes linked to amyloid pathology and improve memory in animal models expands the scientific understanding of therapeutic targets, offering insight into compounds that may help slow down neurodegenerative progression.
This work points toward potential therapeutic or nutraceutical applications targeting neurodegenerative conditions such as Alzheimer's disease. Pharmaceutical developers and health product formulators could explore quercetin formulations, but the findings remain at an early, pre-clinical stage in animal models, meaning extensive further testing and clinical validation are required before any real-world use.
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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.
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DOI: 10.1080/2314808x.2022.2164136
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