The green tea extract, epigallocatechin gallate (EGCG), may slow the accumulation of proteins that cause Huntington's disease, German scientists have reported.
The news adds to a growing body of science on the health benefits of green tea, with consumption linked to a lower risk of certain cancers, increased weight loss, and protection against Alzheimer's.
Huntington's disease, along with Alzheimer's and Parkinson's, belong to the family of neurodegenerative diseases caused by protein misfolding. The incurable disease is hereditary and has a prevalence of 1 in every 15,000 people. In Germany, about 8,000 cases are currently known, in the UK the figure is reported to be about 5,000, and in the US the figure is about 30,000.
The disease is characterize by jerky, uncontrolled movements, an unsteady gait and grimaces leading to its original common name of Huntington's chorea (from the ancient Greek for "dance").
In 1993, scientists discovered the gene that encodes the mutant protein, the so-called huntingtin protein. A mutation in this protein results in elongation of parts of the protein called polyglutamine chains, which cause the overall huntingtin protein to lose its normal structure. These mutant proteins can not be disposed of by the body and accumulate in the brain of sufferers, eventually being toxic to the nerve cells in the brain.
The new research, led by Professor Erich Wanker from the Max Delbrück Center for Molecular Medicine Berlin-Buch (MDC), looked at the effect on EGCG on the aggregation of these mutant proteins in vitro, and found that the green tea extract could interfere with the very early events of this process.
The research is published in the September issue journal Human Molecular Genetics (Vol. 15, pp. 2743-2751), and presented by Dagmar Ehrnhoefer this week at the international conference "Neurodegenerative diseases: molecular mechanisms in a functional genomic frameworks" in Berlin.
"We demonstrate that the green tea polyphenol epigallocatechin-3-gallate (EGCG) potently inhibits the aggregation of mutant huntingtin protein in a dose-dependent manner," wrote lead author Dagmar Ehrnhoefer.
Professor Wanker's group used laboratory-based experiments to show that the green tea extract inhibited misfolding of the huntingtin protein in vitro, as well as using fruit flies genetically modified to over-express the mutant protein. The latter experiments showed that the degeneration of the flies' photoreceptor and motor function improved.
"These results indicate that modulators of huntingtin misfolding … like EGCG are likely to reduce polyglutamine -mediated toxicity in vivo," concluded Ehrnhoefer.
Further research is needed, particular to discern if the bioactive doses needed to produce these protective effects could be obtained from drinking green tea, or by taking supplements.
The researchers themselves appear to be heading down a pharmaceutical route. Nevertheless, the results are in-line with a growing body of research that reports neuroprotective effects of green tea and its extracts.
Green tea is said to contain over four times the concentration of antioxidant catechins than black tea (green tea leaves that have been oxidized by fermentation), about 70 mg catechins per 100 mL compared to 15 mg per 100 mL for black tea.
Consumer awareness of the benefits of green tea and green tea extracts continues to rise with growing numbers of studies, from 430 papers in 2000 to almost 1500 in 2003, reporting benefits of the main compounds, catechins.
This has seen European demand surge, having reached 500 metric tonnes in 2003. Companies such as DSM, with its Teavigo boasting 95 per cent purity of epigallocatechin gallate (EGCG), and Taiyo International, with its Sunphenon claiming more than 90 per cent purity, position themselves firmly in specific catechin markets.