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Myricetin and brai health

Excitotoxicity is the pathological process by which nerve cells are damaged by glutamate, when receptors for the excitatory neurotransmitter glutamate, such as the NMDA receptor, are overactivated. Excitotoxins, high levels of glutamate, reactive oxygen species generation or caspase-3 activation can cause excitotoxicity by allowing high levels of calcium ions to enter the cell. The high level of calcium in the cells activates a enzymes that can damage cell structures, resulting in diseases such as Alzheimer. A study conducted by Y Shimmyo and coworkers at Kyoto University showed that myricetin was a potent anti-neurodegenerative compound and may contribute to the discovery of a drug against neurodegeneration [1]. The scientists came to that conclusion after investigating the effect of myricetin on neurons. They found that myricetin reduced the excitotoxicity by different pathways. Myricetin modulated the NMDA receptor by phosphorylation, resulting in a reduced intracellular calcium level. Myricetin also inhibited ROS production caused by glutamate and reduced glutamate-induced activation of caspase-3.

A study by the Qingdao University, China, concluded that myricetin had protective effect on the toxicity of neurotoxin 6-hydroxydopamine by suppressing iron toxicity [2]. The main use of 6-hydroxydopamine is to induce Parkinsonism in laboratory animals to test new medicines for treating Parkinson's disease in humans. The scientists studied the effects of myricetin on 6-hydroxydopamine-induced neurodegeneration in the substantia nigra-striatum system and found that myricetin restored the dopamine content in the striatum.

[1] Three distinct neuroprotective functions of myricetin against glutamate-induced neuronal cell death: involvement of direct inhibition of caspase-3. J Neurosci Res. 2008 Jun;86(8):1836-45
[2] Myricetin reduces 6-hydroxydopamine-induced dopamine neuron degeneration in rats. Neuroreport. 2007 Jul 16;18(11):1181-5.

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