Background: Oxidative stress and neuronal damage are common factors in the development of neurodegenerative disorders. Myricetin is a flavonoid compound found in various plant-based foods, such as berries, onions, and tea. It possesses potent antioxidant properties due to its ability to scavenge free radicals and inhibit oxidative processes. Myricetin can directly neutralize ROS and enhance the activity of endogenous antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). By reducing oxidative stress, myricetin may help protect neurons from damage in Alzheimer's disease. In view of the given background, the present study has investigated the effect of Myricetin on free radical products formation, in vitro acetylcholinesterase activity and amyloid beta peptide formation. Materials and methods: The study has utilized in vitro enzyme inhibitory assay system to evaluate the antioxidant and neuroprotective potential of Myricetin. The DPPH assay assessed the free radical scavenging activity of the Myricetin. Further, the ABTS radical scavenging activity of Myricetin was determined. Xanthine oxidase inhibitory activity was assessed spectrophotometrically. Ascorbic acid was used as standard to compare the antioxidant effect of Myricetin. The inhibitory potential of Myricetin on in vitro acetylcholinesterase (AchE) activity and amyloid peptide aggregation were evaluated at various concentrations and compared with standard Donepezil hydrochloride. Results: Myricetin exhibited significant antioxidant properties, reduces Aβ aggregation thereby attenuates neuroinflammation. These characteristics make myricetin a promising compound for targeting oxidative stress and neurodegeneration in Alzheimer's disease. However, more research is required to fully understand its therapeutic potential and translate these findings into effective treatments Conclusion: In summary, the present study findings have demonstrated that myricetin can attenuate amyloid-beta (Aβ) aggregation, which is a hallmark pathological feature of AD. Myricetin has been shown to inhibit the formation of Aβ fibrils as well as inhibit AChE activity. These effects are crucial for preventing the formation of amyloid plaques and preserving neuronal function.