Kuo, Li-Chen Song, Yan-Qing Yao, Chien-An H. Cheng, Irene Chien, Chiang-Ting Lee, Guan-Chiun Yang, Wen-Chin Lin, Yenshou Ginkgolide A Prevents the Amyloid-β-Induced Depolarization of Cortical Neurons Utilizing the <i>N</i>-methyl-d-aspartate (NMDA) receptor antagonist as a strategy, memantine is the only agent available for clinically treating mild to severe Alzheimer’s disease (AD). Our aim was to develop novel similar herb-based drugs. Using a screening platform, ginkgolide A (GA), a pure compound extracted from Ginkgo biloba, was found to attenuate amyloid β (Aβ)-induced abnormal depolarization in mouse primary cortical neurons. Using receptor agonists, it was determined that GA inhibits both NMDA receptors and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. Furthermore, the Aβ-induced increase in c-Jun N-terminal kinase phosphorylation in neurons was prevented by GA. Body weight, glutamate oxaloacetate transaminase, glutamic–pyruvic transaminase, liver histology, and kidney histology were similar when the wild-type/AD animal model mice with and without GA treatment were compared. This pure compound improves the memory of wild-type mice. Our findings indicate that GA has great potential clinically for the treatment of AD because it might target NMDA receptors just like memantine. c-Jun N-terminal kinase phosphorylation;GA;compound;histology;attenuate amyloid β;-3-hydroxy acid receptors;wild-type;neuron;NMDA receptors;Cortical Neurons Utilizing;glutamate oxaloacetate transaminase;Amyloid -β-Induced Depolarization;AD;memantine 2018-12-12
    https://acs.figshare.com/articles/journal_contribution/Ginkgolide_A_Prevents_the_Amyloid-_-Induced_Depolarization_of_Cortical_Neurons/7499489
10.1021/acs.jafc.8b04514.s001