Soy Isoflavone Glycitein Protects Against
Beta Amyloid-induced Toxicity and
Oxidative Stress in Transgenic
Caenorhabditis Elegans

This section is compiled by Frank M. Painter, D.C.
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FROM: BMC Neuroscience 2005 (Aug 25);   6:   54 ~ FULL TEXT

Gutierrez-Zepeda A, Santell R, Wu Z, Brown M, Wu Y,
Khan I, Link CD, Zhao B, Luo Y

Department of Biological Sciences,
University of Southern Mississippi,
Hattiesburg, MS 39406, USA.

BACKGROUND:   Epidemiological studies have associated estrogen replacement therapy with a lower risk of developing Alzheimer's disease, but a higher risk of developing breast cancer and certain cardiovascular disorders. The neuroprotective effect of estrogen prompted us to determine potential therapeutic impact of soy-derived estrogenic compounds. Transgenic Caenorhabditis elegans, that express human beta amyloid (Abeta), were fed with soy derived isoflavones genistein, daidzein and glycitein (100 microg/ml) and then examined for Abeta-induced paralysis and the levels of reactive oxygen species.

RESULTS:   Among the three compounds tested, only glycitein alleviated Abeta expression-induced paralysis in the transgenic C. elegans. This activity of glycitein correlated with a reduced level of hydrogen peroxide in the transgenic C. elegans. In vitro scavenging effects of glycitein on three types of reactive oxygen species confirmed its antioxidant properties. Furthermore, the transgenic C. elegans fed with glycitein exhibited reduced formation of beta amyloid.

CONCLUSION:   These findings suggest that a specific soy isoflavone glycitein may suppress Abeta toxicity through combined antioxidative activity and inhibition of Abeta deposition, thus may have therapeutic potential for prevention of Abeta associated neurodegenerative disorders.

The Background Theory and How Soy May Be Able to Help

Testing the Amyloid Toxicity Hypothesis of Alzheimer's Disease in Transgenic Caenorhabditis elegans Model

FROM: Frontiers in Bioscience 2004 (Sep 1);   9:   3333-3338

Alzheimer's disease (AD) is affecting more people every year due to the increase in elderly population. This disease is characterized by senior plaques, containing aggregated amyloid beta peptide (A beta), and neurofibrillary tangles in the AD brains. The A beta depositions are thought to increase in cellular oxidative stress, which subsequently produces neuronal cell death in the patient's brain, causing loss of memory and, in the latter stages, dementia. Diverse models have been established to test this, "Amyloid Toxicity Hypothesis of AD". Among these, the use of the nematode Caenorhabditis elegans has some advantages. This invertebrate has its entire genome known, as well as numerous gene homologues to those seen in humans. In relationship with the cell model, the nematode gives the benefit of an organismal view of the disease. The nematode's short life span proves useful, when compared with that of mice, allowing mechanistic studies of the disease and pharmacological treatments. Alongside with other laboratories, we have used this in vivo model to correlate the Abeta expression with its toxicity through the observance of the organism's behavior to provide a better understanding of the cellular processes underlining AD.

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