Ginkgolide A Prevents the Amyloid-β-Induced Depolarization of Cortical Neurons

Li Chen Kuo, Yan Qing Song, Chien An Yao, Irene H. Cheng, Chiang Ting Chien, Guan Chiun Lee, Wen Chin Yang, Yenshou Lin*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

26 Citations (Scopus)


Utilizing the N-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.

Original languageEnglish
Pages (from-to)81-89
Number of pages9
JournalJournal of Agricultural and Food Chemistry
Issue number1
Publication statusPublished - 2019 Jan 9


  • Alzheimer's disease
  • amyloid β
  • ginkgolide A
  • glutamate receptors
  • herbal medicines
  • memantine

ASJC Scopus subject areas

  • General Chemistry
  • General Agricultural and Biological Sciences


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