Extract from the Ginko Biloba Leaf has been used in Europe and China to treat a variety of conditions, most notably Memory Loss and Dementia. Although the Ginkgo Species is very old, having survived for 200-300 million years, the standardized extract is relatively new ~20 years. A recent article published in the Journal of the American Medical Association confirms that Ginkgo Biloba Extract is an important new tool in treating Memory Loss and Dementia.
A Placebo-Controlled, Double-blind, Randomized Trial of an Extract of Ginko Biloba for Dementia
Authors: Pierre L. Le Bars, MD, PhD; Martin M. Katz, PhD; Nancy Berman, PhD; Turan M. Itil, MD;Alfred M. Freedman, MD; Alan F. Schatzberg, MD; for the North American EGb Study Group
Journal of the American Medical Association, October 22/29, 1997-Vol 278: 1327-1332Context: EGb 761 is a particular extract of Ginkgo Biloba used in Europe to allviate symptoms associated with numerous cognitive disorders. Its use in dementia is based on the positive results from only a few controlled clinical trails, most of which did not include standard assessments of cognitive behavior.
Objective: To assess the efficacy and safety of EGb in Alzheimer disease and multi-infarct dementia.
Design: A 52-week, randomized double blind, placebo-controlled, parrallel-group, multicenter study.
Patients. Mildly to severely demented outpatients with Alzheimer disease or multi-infarct dementia, without significant other medical conditions.
Intervention.- Patients assigned randomly to treatment with EGb (120 mg/d) or placebo. Safety, compliance, and drug dipensation were monitored every 3 months with complete outcome evaluation at 12, 26, and 52 weeks.
Primary Outcome Measures: Alzheimer's Disease Assessment Scale-Cognitive subscale (ADAS-Cog), Geriatric Evaluation by Relative's Rating Instrument (GERRI), and Clinical Global Impression of Change (CGIC).
Results: From 309 patients included in the intent-to-treat analysis, 202 provided evaluable data for the 52-week end point analysis. In the intent to treat analysis, the EGb group had an ADAS-Cog Score 1.4 points better than the placebo group (P=.04) and a GERRI score 0.14 points better than the placebo group (P=.004). The same patterns were observed with the evaluable data set in which 27% of patients treated with EGb achieved at least a 4-point improvement on the ADAS-Cog, compared with 14% taking placebo (P.005); on the GERRI, 37% were considered improved with EGb, compared with 23% taking placebo (P=.003). No differenc was seen in the CGIC. Regarding the safety profile of EGb, no significant differences compared with placebo were observed in the number of patients reporting adverse events or in the incidence and severity of these events.
Conclusions: EGb was safe and appears capable of stabilizing and, in a substantial number of cases improving the cognitive performance and the social functioning of demented patients for 6 months to 1 year. Although modest, the changes induced by EGb were objectively measured by the ADAS-Cog and were of sufficient magnitude to be recognized by the caregivers in the GERRI.
