2. Academic Validation
  3. Protection against beta-amyloid induced abnormal synaptic function and cell death by Ginkgolide J

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

Affiliation

  • 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.

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