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Mitochondrial effects of Ginkgo biloba extract

Published online by Cambridge University Press:  12 July 2012

Anne Eckert*
Affiliation:
Neurobiology Laboratory for Brain Aging and Mental Health, Psychiatric University Clinics, Basel, Switzerland
*
Correspondence should be addressed to: Anne Eckert, Neurobiology Laboratory for Brain Aging and Mental Health, Assoc. Res. Group Dept. Biomedicine Univ. of Basel, Psychiatric University Clinics Basel, Wilhelm Klein-Strasse 27, CH-4025 Basel, Switzerland. Phone: +41 61 325 54 87, Fax: +41 61 325 55 77. Email: anne.eckert@upkbs.ch.

Abstract

Oxidative stress and mitochondrial failure promote altered protein degradation, reduced neurotransmission, synapse loss and tau/hyperphosphorylation, which are early stages in the development of Alzheimer's disease (AD). A growing volume of data confirms that Ginkgo biloba extract (GBE) reduces oxidative stress and improves mitochondrial respiration and thus may be useful in preventing or slowing down the progression of AD. Treatment of Caenorhabditis elegans with GBE- extract reduces oxidative stress and extends median lifespan compared with controls. Levels of reactive oxygen species, including the superoxide anion radical, were reduced in brains from GBE-treated mice compared with controls. In older mice, GBE resulted in a protective effect by increasing production of adenosine triphosphate in neurons. A respiratory experiment indicated that GBE was able to rescue Aβ-induced defects in energy metabolism, with results suggesting long-term regulatory effects on mitochondria. GBE also had a selective effect on the activities of mitochondrial enzymes that assemble the electron transport system. The flavonoids, bilobalide and some of the ginkgolides (B and J) had a high protective capacity, indicating that a combination of several compounds within standardized Gingko biloba extracts contribute disproportionately for these protective effects.

Type
Research Article
Copyright
Copyright © International Psychogeriatric Association 2012

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