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aDepartment of Pharmacology, Biocenter, University of Frankfurt, 60439, Frankfurt, Germany bNeurobiology Research Laboratory, Psychiatric University Clinic, 4025 Basel, Switzerland
Address for correspondence: Anne Eckert, Neurobiology Research Laboratory, Psychiatric University Clinic Basel, CH-4025 Basel, Switzerland. Voice: +41 61 325 5487; fax: +41 61 325 5577. anne.eckert{at}upkbs.ch
Ginkgo biloba extract EGb 761 has been used for many years to treat age-related cognitive disorders including Alzheimer's disease. EGb 761 given shortly after initiating mitochondrial damage by sodium nitroprusside (nitric oxide donor) improved the mitochondrial membrane potential of PC12 cells significantly and dose dependently. Under these conditions, EGb 761 also reversed the decrease in ATP production. In addition, similar protection against oxidative damage was found in dissociated brain cells and isolated brain mitochondria after in vitro or in vivo treatment with EGb 761. Moreover, PC12 cells bearing an Alzheimer's disease-related mutation in the amyloid precursor protein, which leads to enhanced beta amyloid production, showed greater benefit from treatment with EGb 761 than did control cells. Taken together, our findings clearly show stabilization and protection of mitochondrial function as a specific and very sensitive property of EGb 761 at therapeutically relevant doses.
Key Words: Ginkgo biloba • mitochondria • energy metabolism • Alzheimer's disease • aging • oxidative stress
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