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Green Tea Antioxidant May Help Prevent Alzheimer's
Date:5/30/2008

The science looks hopeful, but it's still too early to make a dietary recommendation, experts say

FRIDAY, May 30 (HealthDay News) -- An antioxidant found in green tea appears to prevent the development of amyloid fibrils, a toxic protein associated with Alzheimer's and Parkinson's disease, a new study finds.

Amyloid plaque is commonly seen in the brains of Alzheimer's patients and appears to disrupt the function of cells. Strategies to prevent the development of amyloid plaque are one avenue being explored in the prevention and treatment of Alzheimer's.

Now, a German team says the tea antioxidant, called epigallocatechin gallate (EGCG), has potent anti-plaque ability.

"We can use small molecules like EGCG to convert certain misfolded structures of a protein into a new type of molecule, which is less toxic or not toxic for cells," said lead researcher Erich Wanker, from the Max Delbrueck Center for Molecular Medicine in Berlin.

The findings are published in the May 30 online edition of Nature Structural & Molecular Biology.

The accumulation of amyloid plaque in Alzheimer's and other neurodegenerative diseases, such as Parkinson's, are thought to be caused by the misfolding of certain proteins, which then become toxic to cells. The way proteins fold is key to their function, the researchers explained.

In experiments in the laboratory, the German team found that EGCG seems to change potentially harmful proteins into proteins that are not detrimental to brain cells. "We are able to convert a toxic structure into a less toxic structure," Wanker explained.

Because EGCG binds to unfolded proteins -- which are not associated with Alzheimer's -- the discovery could lead to medications that recognize the more troublesome proteins and convert them to harmless substances.

"This method could be more generally used to get rid of or remove the concentration of misfolded proteins in cells," Wanker said. "This strategy should be tested with patients. If treated early on, it could prevent the formation of amyloid plaque," he speculated.

Whether this type of treatment could reverse plaques that have already formed in the brain isn't known, Wanker said.

He noted that the study remains basic science, and he was cautious about recommending green tea as a way of preventing Alzheimer's disease. "I don't want to do a lot of speculating which could point people in the direction that could be harmful," Wanker said. "We have to go step-by-step."

One expert believes the approach could yield real results, however.

"Red wine, yellow curry and green tea have suspected health benefits because of high content of antioxidants," said Greg M. Cole, a neuroscientist at the Greater Los Angeles VA Healthcare System, and associate director of the Alzheimer's Disease Research Center at UCLA David Geffen School of Medicine. He was not involved in the study.

"This study provides evidence that a compound called EGCG, one of the major polyphenols in green tea, may be useful for diseases like Parkinson's and Alzheimer's, because it can block the formation of the filament-forming protein aggregates implicated in causing disease," Cole said.

One novel aspect of the study is the authors' demonstration that EGCG prevents toxic filament formation by redirecting the aggregating proteins to make non-toxic proteins, Cole said.

"This is surprising, because similar protein aggregate spheres called amyloid oligomers can be highly toxic to neurons and synapses," Cole said. "It will be important for the authors to prove that the EGCG-directed proteins also lack toxicity to synapses which were not present in the systems used to test toxicity," he said.

Assuming that the green tea compound has a stable effect and chronically blocks toxicity to real neurons and synapses, it could have genuine potential for Alzheimer's patients, Cole said.

"The major caveat is the very poor absorption and delivery of EGCG seen in some studies," Cole said. The fact that EGCG isn't available for patenting by pharmaceutical companies might be a problem, too, he said, since it could "limit the investment needed for clinical trials of sufficient size to prove that it really works."

In related research, a team of American scientists said that interrupting a key signaling pathway in immune system cells allowed those cells to enter the brain and attack and remove amyloid plaque.

Reporting May 30 in Nature Medicine, a team led by research scientist Terrence Town, of Cedars-Sinai Medical Center, Los Angeles, conducted their study in genetically engineered mice. The group blocked a molecule that typically suppresses a portion of the immune response. Once the system was freed up, immune cells called macrophages made their way to the brains and devoured up to 90 percent of amyloid plaques, the team said.

"If these experimental animals are representative of the clinical syndrome of Alzheimer's disease, we may have a therapeutic target that we did not have before," study co-author Dr. Jun Tan, of the University of South Florida, said in a statement.

More information

For more about Alzheimer's disease, visit the Alzheimer's Association.



SOURCES: Erich Wanker, Ph.D., Max Delbrueck Center for Molecular Medicine, Berlin, Germany; Greg M. Cole, Ph.D., neuroscientist, Greater Los Angeles VA Healthcare System, and associate director, Alzheimer's Disease Research Center, UCLA David Geffen School of Medicine; May 30, 2008, online edition, Nature Structural & Molecular Biology; May 30, 2008, statement, Cedars-Sinai Medical Center, Los Angeles


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