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Ginkgo May Enhance Cognitive Health

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By VRP Staff

Ginkgo biloba suppressed pathological behaviors associated with the destructive protein known as amyloid-beta, and prevented its toxicity in an in vivo model of Alzheimer’s disease.

Amyloid-beta toxicity has been postulated to initiate the synaptic loss and subsequent neuronal degeneration seen in Alzheimer's disease (AD). The researchers of the current study had previously demonstrated that a standardized Ginkgo biloba extract inhibits amyloid-beta-induced cell death in neuroblastoma cells.

In this study, researchers used ginkgo and its single constituents to study amyloid-beta and amyloid-beta-induced pathological behaviors in Caenorhabditis elegans, a worm that served as a model organism. The results indicated that ginkgo and one of its components, ginkgolide A, alleviates amyloid-beta-induced pathological behaviors, including paralysis. In addition, the ginkgo reduced the process known as chemotaxis, the movement of additional white blood cells to an area of inflammation in response to chemical mediators. Furthermore, the ginkgo inhibited amyloid-beta deposits.

The researchers also tested ascorbic acid (vitamin C) and found that even though the ascorbic acid reduced intracellular levels of hydrogen peroxide (a harmful pro-oxidant) to the same extent as ginkgo, it was not nearly as effective as ginkgo in suppressing paralysis. Consequently, they concluded that oxidative stress reduction is not the mechanism by which ginkgo and ginkgolide A suppress amyloid-beta paralysis.

The study authors concluded that their findings suggest that ginkgo
suppresses amyloid-beta-related pathological behaviors and that ginkgo and ginkgolide A have “therapeutic potential for prevention and treatment of Alzheimer’s.”

Reference:
Wu Y, Wu Z, Butko P, Christen Y, Lambert MP, Klein WL, Link CD, Luo Y. Amyloid-�-Induced Pathological Behaviors Are Suppressed by Ginkgo biloba Extract EGb 761 and Ginkgolides in Transgenic Caenorhabditis elegans. The Journal of Neuroscience. December 13, 2006; 26(50):13102-13113. [E pub Ahead of Print].