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Herbs for early stage dementia

Ginkgo is the world's oldest living species of tree, with fossil records dating back more than 200 million years. It is the lone survivor of the Ginkgoaceae family and individual trees may live as long as 1,000 years. Ginkgo trees can grow as high as 80 to 125 feet and produce characteristic fan-shaped leaves. The leaves of younger, cultivated trees are used in modern herbal preparations.

Medicinal use of ginkgo can be traced back almost 5,000 years in traditional Chinese medicine. Ginkgo was first introduced in the pharmacopoeia, Chen Noung Pen T'sao. The leaves were recommended for asthma and chilblains as well as memory loss in the elderly. The seeds were considered a digestive aid and a deterrent to drunkenness.

Spearheaded by the Dr. Wilmar Schwabe phytopharmaceutical company of Karlsruhe, Germany, twenty years of research resulted in a concentrated, standardized extract of ginkgo leaves known generically as EGb 761. Today, ginkgo extracts (GBE) exist on the European market in both parenteral and intravenous forms. GBE is the most frequently prescribed phytomedicine in Europe today. Its impressive track record of more than 400 pharmacological and clinical studies and reports also make it the best researched phytomedicine in the world.

Active Constituents

Most critical to the extraction process and final phytomedical product is the standardization of two groups of active constituents--the terpene lactones and ginkgo flavone glycosides. High quality GBE is typically standardized on 24% ginkgo flavone glycosides and 6% terpene lactones. The primary terpene lactones in GBE are the three ginkgolides A, B, and C, as well as bilobalide . The actions of these constituents include neuroprotection, improvement in circulatory perfusion and in the rheological properties of the blood, inhibition of platelet-activating factor (PAF), and cognitive activation. The flavone glycosides are typically a carefully measured balance of quercetin, kaempferol and isorhamnetin . These constituents are responsible for the antioxidant properties of GBE as well as mild inhibition of platelet aggregation.

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Mechanism of Action

Improvement of hypoxic tolerance, particularly the cerebral tissue

Inhibition in the development of traumatically or toxically produced cerebral edema and acceleration of decongestion