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Green tea ingredient prevents Alzheimer's-like brain damage in mice

Tampa, FL (Sept. 21, 2005) -- Researchers at the University of South (USF) have found that green tea may offer another potential health benefit -- protecting the brain against the ravages of Alzheimer's disease.

In an article published Sept. 21 in the Journal of Neuroscience, USF researchers report that a component of green tea prevented Alzheimer's-like damage in the brains of mice genetically programmed to develop the neurodegenerative disease process. The component, called epigallocatechin-3-gallate (EGCG), is a major antioxidant in green tea and has been widely studied for its reported protection against certain cancers.

Now the USF team provides the first evidence that EGCG decreases production of the Alzheimer's-related protein, beta-amyloid, which can accumulate abnormally in the brain and lead to nerve damage and memory loss. This reduction in beta-amyloid was observed both in cell cultures and a mouse model for Alzheimer's disease. EGCG appears to block the initial process by which the Alzheimer's-related protein is formed in brain cells.

After treating Alzheimer's mice for several months with daily injections of pure EGCG, the researchers observed a dramatic decrease -- as much as 54 percent -- of brain-clogging Alzheimer's plaques.

"The findings suggest that a concentrated component of green tea can decrease brain beta-amyloid plaque formation," said senior study author Jun Tan, PhD, MD, director of the Neuroimmunology Laboratory at the Silver Child Development Center, USF Department of Psychiatry. "If beta-amyloid pathology in this Alzheimer's mouse model is representative of Alzheimer's disease pathology in humans, EGCG dietary supplementation may be effective in preventing and treating the disease."

Green tea contains many antioxidants, including those known as flavonoids that can protect against free radical damage to the brain. However, Dr. Tan and colleagues demonstrated that other flavinoids in green tea actually oppose naturally-occurring EGCG's ability to prevent the harmful build-up of beta-amyloid. Thus, Dr. Tan said, drinking green tea alone would not likely have a beneficial effect through the same mechanism that EGCG works.

"This finding suggests that green tea extract selectively concentrating EGCG would be needed to override the counteractive effect of other flavinoids found in green tea," said study co-author Doug Shytle, PhD. "A new generation of dietary supplements containing pure EGCG may lead to the greatest benefit for treating Alzheimer's disease." Dr. Tan said humans would likely need 1500 to 1600 mg of EGCG daily to approximate the injection dosage that benefited the Alzheimer's mice. That dosage has already been studied in healthy human volunteers and was found to be safe and well tolerated.

The USF researchers plan to study whether multiple oral doses of EGCG can improve memory loss in Alzheimer's mice as well as reducing their Alzheimer's plaque burden. "If those studies show clear cognitive benefits," Dr. Tan said, "we believe clinical trials of EGCG to treat Alzheimer's disease would be warranted."

Kavon Rezai-Zedah, a PhD candidate in the USF Department of Medical Microbiology and Immunology was first author of the study. Other authors were Nan Sun, MS; Takashi Mori, PhD, Huayan Hou, MD; Deborah Jeanniton, BS; Jared Ehrhart; PhD candidate; Kirk Townsend, PhD; Jin Zeng, MS; David Morgan, PhD; John Hardy, PhD; and Terrence Town, PhD.

The study was supported by the Johnnie B. Byrd Sr. Alzheimer's Center & Research Institute, USF College of Medicine faculty start-up funds, the National Institute of Neurological Disorders and Stroke and the Alzheimer's Association.