Protection against beta-amyloid induced abnormal synaptic function and cell death by Ginkgolide J

  • Neurobiol Aging. 2009 Feb;30(2):257-65. doi: 10.1016/j.neurobiolaging.2007.05.025.
Ottavio Vitolo  1 ,  Bing Gong ,  Zixuan Cao ,  Hideki Ishii ,  Stanislav Jaracz ,  Koji Nakanishi ,  Ottavio Arancio ,  Sergei V Dzyuba ,  Roger Lefort ,  Michael Shelanski
Affiliations
  • 1. Department of Pathology and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.
PMID: 17640772 DOI: 10.1016/j.neurobiolaging.2007.05.025
Abstract

A new Ginkgo biloba extract P8A (TTL), 70% enriched with terpene trilactones, prevents A beta(1-42) induced inhibition of long-term potentiation in the CA1 region of mouse hippocampal slices. This neuroprotective effect is attributed in large part to ginkgolide J that completely replicates the effect of the extract. Ginkgolide J is also capable of inhibiting cell death of rodent hippocampal neurons caused by A beta(1-42). This beneficial and multi-faceted mode of action of the ginkgolide makes it a new and promising lead in designing therapies against Alzheimer's disease.

Products