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Alzheimer's Disease
Updated: 05/21/2003

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http://altmed.creighton.edu/ginkgo/science.htm
Research for the Use of Ginkgo Biloba in Treating Alzheimers Disease

There was a recent article in the Feb. 2000 issue of Free Radical Research written by Kobayashi, M.S., Han, D., and Packer, L., that suggested that certain herbal extracts may be beneficial antioxidants in neurological disorders including Alzheimer’s disease. Their research showed that purified flavonoids, herbal extracts of Ginkgo biloba (EGb 761) and French maritime pine bark (Pycnogenol) were effective in protecting neuronal cells against glutamate-induced cytotoxicity in HT-4 neuronal cells.

Another article in the September 1999 issue of Free radical biology and medicine supported the use of antioxidants for protection in the frontal cortex of Alzheimer’s patients whose oxidative damage is related to the apolipoprotein E genotype. An increasing number of epidemiological studies are demonstrating the frequency of the epsilon 4 allele of the apolipoprotein E gene (APOE) is markedly higher in sporadic and familial late onset Alzheimer’s disease. The research was done to address the hypothesis that the apoE4 genotype and reactive oxygen-mediated damage are linked in the frontal cortex of Alzheimer disease patients. The Ginkgo biloba extract (EGb 761), the neurosteroid dehydroepiandrosterone (DHEA) and human recombinant apoE3 were able to protect Alzheimer disease patients that were homozygous epsilon3/epsilon3 and heterozygous epsilon3/epsilon4, against hydrogen peroxide/iron-induced lipid oxidation. However EGb 761 and DHEA had no effect in homozygous epsilon4 cases.

A formal review of current literature was done in 1998 by Oken, B.S., Storzbach, D.M., and Kaye, J.A., to determine the effect of treatment with Ginkgo biloba extract on objective measures of cognitive function in patients with Alzheimer Disease. The attempted to identify all English and non-English-language articles in which Ginkgo biloba extract was given to subjects with dementia or cognitive impairment. In order to be included in the meta-analysis (1) the patients had to be sufficiently characterized such that is was clearly stated that there was a diagnosis of Alzheimer disease by either Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition, or National Institute of Neurological Disorders and Stroke Alzheimer’s disease and Related Disorders Association criteria, or there was enough clinical detail to determine this by our review; (2) Studies that did not have stated exclusion for depression, other neurological disease, and central nervous system-active medications were excluded; (3) use of standardized ginkgo extract in any stated dose; (4) randomized, placebo-controlled and double-blinded study design; (5) at least 1 outcome measure was an objective assessment of cognitive function; and (6) sufficient statistical information to allow for meta-analysis. Of the articles reviewed only 4 studies met all inclusion criteria giving a total of 212 subjects in each of the placebo and ginkgo treatment groups. The meta-analysis showed an overall significant effect size of 0.40 (P<.0001). This effect size translated into a 3% difference in the Alzheimer Disease Assessment Scale-cognitive subtest. The article concluded that there was a small but significant effect of 3- to 6-months of treatment with 120 to 240 mg of Ginkgo biloba extract on objective measures of cognitive function in Alzheimer disease. The article also stated that at the present time there is limited and inconsistent data to determine if there are effects on non-cognitive behavioral and functional measures as well as clinician’s global rating scales. They also concluded that additional research is needed to determine the best dosage as well as research to define which ingredients in the ginkgo extract are producing its effects in individuals with Alzheimer’s disease.

Another placebo-controlled, double-blind, randomized trial of an extract of Ginkgo biloba for the treatment of dementia was conducted by LeBars, P.L., katz, M.N., Berman, N., Itil, T.M., Freedman, A.M., and Schatzberg, A.F., and published in the Journal of American Medical Association. The objective of the article was to assess the efficacy and safety of EGb 761 in Alzheimer’s disease and multi-infarct dementia. The patients in the trial were mildly to severely demented outpatients with the diagnosis of Alzheimer disease or multi-infarct dementia, without other significant medical conditions. The patients were assigned randomly to treatment with EGb (120 mg/d) or placebo. Drug dispensation, safety, and compliance were monitored every 3 months with complete outcome evaluation at 12, 26, and 52 weeks. The outcome measures used were the Alzheimer’s Disease Assessment Scale-Cognitive subscale (ADAS-Cog), Geriatric Evaluation by relative’s Rating Instrument (GERRI), and Clinical Global impression of Changes (CGIC). The authors of the study concluded that EGb was safe and was 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 in comparison to placebo. Although the changes were modest, the changes induced by EGb were objectively measured by the ADAS-Cog and were of satisfactory magnitude to be recognized by the caregivers in the GERRI.



I take pycnogenol along with several other plant based antioxidants DAILY.

1: Veurink G, Liu D, Taddei K, Perry G, Smith MA, Robertson TA, Hone E, Groth DM, Atwood CS, Martins RN. Related Articles, Links
Reduction of inclusion body pathology in ApoE-deficient mice fed a combination of antioxidants.
Free Radic Biol Med. 2003 Apr 15;34(8):1070-7.
PMID: 12684092

2: Peng QL, Buz'Zard AR, Lau BH. Related Articles, Links
Pycnogenol protects neurons from amyloid-beta peptide-induced apoptosis.
Brain Res Mol Brain Res. 2002 Jul 15;104(1):55-65.
PMID: 12117551

3: Liu F, Lau BH, Peng Q, Shah V. Related Articles, Links
Pycnogenol protects vascular endothelial cells from beta-amyloid-induced injury.
Biol Pharm Bull. 2000 Jun;23(6):735-7.
PMID: 10864026

4: Kobayashi MS, Han D, Packer L. Related Articles, Links
Antioxidants and herbal extracts protect HT-4 neuronal cells against glutamate-induced cytotoxicity.
Free Radic Res. 2000 Feb;32(2):115-24.
PMID: 10653482