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

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.

• Authors: Ottavio Vitolo, Bing Gong, Zixuan Cao, Hideki Ishii, Stanislav Jaracz, Koji Nakanishi, Ottavio Arancio, Sergei V Dzyuba, Roger Lefort, Michael Shelanski
• Journal: Neurobiology of aging (Neurobiol Aging) Vol. 30 Issue 2 Pg. 257-65 (Feb 2009) ISSN: 1558-1497 [Electronic] United States
• PMID: 17640772 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)

Chemical References

• Amyloid beta-Peptides
• Ginkgolides
• Lactones
• Neuroprotective Agents
• Peptide Fragments
• amyloid beta-protein (1-42)
• ginkgolide J

Topics

• Amyloid beta-Peptides (administration & dosage)
• Animals
• Apoptosis (drug effects, physiology)
• Cells, Cultured
• Ginkgolides (administration & dosage)
• Lactones (administration & dosage)
• Mice
• Mice, Inbred C57BL
• Neurons (drug effects, physiology)
• Neuroprotective Agents (administration & dosage)
• Peptide Fragments (administration & dosage)
• Synapses (drug effects, physiology)
• Synaptic Transmission (drug effects, physiology)