Its neuroprotective property in AD majorly involves mitochondrial protection from the toxicity induced by Aβ aggregation. It acts as an NMDA receptor antagonist, reducing glutamate-excite toxicity and minimizing the level of synaptic loss with neuronal cell death. It has been shown to reduce the BDNF level in patients with AD and mild cognitive impairment. It also presents AChE-inhibitory activity. It is clinically approved in China. The gene discussed is ACHE; the disease is Cognitive impairment.