reviewed by X. Li, Ph. D.
(credential)
Alzheimer's disease is a neurodegenerative disease that affects 4 millions of people in USA.
The main symptom of Alzheimer's disease is dementia, a progressive loss of cognition or memory.
Former US president Ronald Reagen who is suffering Alzheimer's disease cannot even recognize
his wife Nancy. Currently no treatment has been found to cure
Alzheimer's disease or to efficiently halt its progression.
As ginkgo biloba is found to contain a strong antioxidation activity and to improve
microcirculation in the brain, it may provide a strong neuroprotective function. Extensive
clinical trials have been conducted to study the benefit of ginkgo biloba
on Alzheimer's disease. These clinical studies in general found that ginkgo biloba extract
can slow down the progression of dementia of Alzheimer's disease and even slightly improve
dementia in some Alzheimer's disease patients and are reviewed in
Ginkgo Biloba for Alzheimer's Disease
Dementia and Multi-Infarct Dementia.
Other laboratory studies have tried to find the underlying basis for ginkgo biloba's action on
Alzheimer's disease. Several recently published studies1-3 revealed multiple effects of ginkgo
which are consistent with its benefits on Alzheimer's disease. These effects include
inhibition of b-amyroid deposition, protection of neurons from cell death, and
regulation of genes in the brain.
Inhibition of b-amyroid deposition
A major hallmark of Alzheimer's disease is the occurrence of amyloid plaques in the brain
of patients. The plaques result from the deposition of insoluble amyloid b
peptide outside of the nerve cells and are believed to be a main cause of Alzheimer's disease.
When amyloid b peptides are purified and left in
solution, they can aggregate and form fiber-like bundles. Similar aggregation also occurs when amyloid
b peptides are produced and secreted from neuronal cells
in culture dishes. This aggregation mimics what happens in the brain of Alzheimer's disease patients.
Now when researchers added the standardized ginkgo biloba extract into the test tube or culture
dishes, they observed the aggregation of amyloid b peptides is
very much prevented1. This result showed the potential effect of ginkgo in reducing
the deposition of amyloid b peptides in the brain.
Protection of neurons from death due to amyloid deposition
Amyloid deposition b is toxic to neurons. Evidence is obtained that
amyloid b peptides induce cell death in neuron cells and thus
contribute to the neuronal degeneration and loss of brain function. In culture dishes, when cells
are engineered to produce and secrete the amyloid b peptides,
the amyloid b peptides initiate a process called programmed
cell death in which mitochondria (a key structure in cells) and many proteins are involved. If
the standardized ginkgo biloba extract was added to the cells, cell death happens significantly
less as shown by much normal mitochondria in treated cells1. Moreover, the activity of
caspase-3, a key protein involved in cell death and whose activity is activated by amyloid
b peptides, is reduced in ginkgo treated cells1.
In a separate study, the standardized ginkgo biloba extract was found to protect neuron cells of
hippocampus in the brain from toxicity induced by the amyloid b
peptides2.
Regulation of genes in the brain
The latest gene chip technology has also been applied to study ginkgo's effect on the brain3.
In this study, mice were fed with the standardized ginkgo biloba extract for 4 weeks. The hippocampus
and cortex from the brain of these mice were then taken for analysis of gene expression by
gene chip technology. Because both hippocampus and cortex are critical for memory and learning,
change in gene expression may give hints to understand how ginkgo acts.
What the researchers found is that several genes are up-regulated, which means they produced more
proteins of the kind. For example, the only gene whose expression is significantly up-regulated in the
hippocampus makes transthyretin. Transthyretin is involved in transport of thyroid hormones which
in turn regulate neuronal growth and development. Transthyretin is also shown to prevent
amyloid b aggregation. It is noteworthy that transthyretin
levels are found much reduced in Alzheimer's disease patients.
Reference
1. Luo Y, Smith JV, Paramasivam V, Burdick A, Curry KJ, Buford JP, Khan I, Netzer WJ,
Xu H, Butko P. Inhibition of amyloid-beta aggregation and caspase-3 activation by the Ginkgo
biloba extract EGb761. Proc Natl Acad Sci U S A. 2002 Sep
17;99(19):12197-202.
2. Bastianetto S, Ramassamy C, Dore S, Christen Y, Poirier J, Quirion R. The Ginkgo biloba extract (EGb 761) protects hippocampal neurons against cell
death induced by beta-amyloid. Eur J Neurosci. 2000
Jun;12(6):1882-90.
3. Watanabe CM, Wolffram S, Ader P, Rimbach G, Packer L, Maguire JJ, Schultz PG, Gohil
K. The in vivo neuromodulatory effects of the herbal medicine ginkgo
biloba. Proc Natl Acad Sci U S A. 2001 Jun 5;98(12):6577-80.
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