Quercetin ameliorates neuroinflammatory and neurodegenerative biomarkers in brain and improves neurobehavioral parameters in repeated intranasal amyloid-beta exposed model of Alzheimer’s disease

Abstract

Objectives: The aim of the present study was to study the potential therapeutic effects of quercetin in protection against repeated intranasal exposure of amyloid-beta-induced mice model. Methods: Mice received intranasal Aβ1-42 (5µg/10µL) exposure once daily for seven consecutive days. Quercetin was orally administered to them at 30 mg/kg and 100 mg/kg doses for one week starting from day five following Aβ1-42 peptide administration. Following this, the animals were evaluated for neurobehavioral parameters in Morris water maze test and Novel object recognition test. Further to this, the biomarkers of neuroinflammation and neurodegeneration biomarkers were evaluated in hippocampus and cortex regions of brain in these animals. Results: Multiple intranasal Aβ exposure led to a significant decline in the learning and cognitive memory of animals, whereas oral treatment with quercetin at 30 and 100mg/kg of dose alleviated Aβ induced effects. Quercetin treatment significantly reduced Aβ accumulation, oxidative stress and proinflammatory cytokines biomarkers in the brain. In addition, it also alleviated activation of astrocytic biomarker, amyloid precursor protein and phosphorylated-tau proteins in the brain. Conclusion: Quercetin was found to be a potent antioxidant, anti-inflammatory compound with protection against neurodegenerative damage and improved learning and cognitive memory in repeated Aβ-exposure model of AD.