德國科學(xué)家報(bào)告稱,，綠茶提取物（Epigallocatechin Gallate）可以減緩體內(nèi)蛋白質(zhì)積累,防止亨廷頓氏癥的發(fā)生,。
越來越多的科學(xué)家認(rèn)為綠茶對人體有益。習(xí)慣飲用綠茶的人，得癌癥的風(fēng)險(xiǎn)較低,。綠茶能夠起到有效的減肥作用,，防止老年癡呆。
亨廷頓疾病,，癡呆證和柏金森疾病等都屬于神經(jīng)性疾病,，是由蛋白質(zhì)突變導(dǎo)致的。這種不治之癥與遺傳有關(guān),。在15,，000人當(dāng)中大約有一人患有此癥。德國目前已知患者約有8000位,。英國提供的患者數(shù)目大約是5000人,，美國為3萬人。
這種疾病的特征是走路顛簸,，平衡力差,，步伐不穩(wěn)。俗稱亨廷頓夜盲癥,。
1993年,，科學(xué)家發(fā)現(xiàn)了揭開蛋白質(zhì)突變密碼的基因，即亨廷頓蛋白質(zhì).,。這一蛋白質(zhì)一旦變異,，便會拉長蛋白質(zhì)鏈,使整個(gè)亨廷頓蛋白質(zhì)失去正常結(jié)構(gòu)。這些突變蛋白質(zhì)人體無法處理,，積聚在患者的大腦中,，最終導(dǎo)致腦神經(jīng)細(xì)胞中毒。
這項(xiàng)新研究是由中心分子醫(yī)學(xué)柏林委員會的Max Delbrück中心的Erich Wanker教授發(fā)起的,。根據(jù)對綠茶提取物（epigallocatechin gallate ）的綜合分析發(fā)現(xiàn),，綠茶提取物會影響蛋白質(zhì)表面的早期活動。
這項(xiàng)研究刊登在九月份的《人類分子遺傳學(xué)》(第15部分,，2743年至2751年),。由Dagmar Ehrnhoefer于本周在名為“神經(jīng)退化疾病，功能基因的分子機(jī)制框架”的國際會議上提出,。
“我們證明綠茶提取物有效地阻止亨廷頓蛋白質(zhì)突變的產(chǎn)生,，”Dagmar Ehrnhoefer稱。
Wanker教授的實(shí)驗(yàn)小組進(jìn)行的實(shí)驗(yàn)表明,，綠茶提取物能夠抑制亨廷頓蛋白質(zhì)的表層活動,，并利用果蠅基因有力的遏制蛋白質(zhì)突變。后續(xù)的實(shí)驗(yàn)中還發(fā)現(xiàn)果蠅的感光和活動能力得到了改善,。
Ehrnhoefer總結(jié)說：“研究結(jié)果表明綠茶提取物能夠降低中介毒性,。”
如果這種活性劑所需的保護(hù)可從綠茶或補(bǔ)充物中獲得,，那么，進(jìn)一步的研究則顯得非常必要,。越來越多的研究報(bào)告提到綠茶及其提取物的益處,。
綠茶中氧化劑濃度據(jù)說比紅茶多出四倍（紅茶是被氧化，發(fā)酵過的綠茶）,。
消費(fèi)者不斷的意識到綠茶及其提取物的益處,，相關(guān)的研究論文也不斷的出現(xiàn)，有關(guān)報(bào)告兒茶酸的研究論文,，從2000年的430篇增加到2003年的1500篇,。
在歐洲，茶需求量不斷增長,，2003年已達(dá)500公噸,。DSM公司聲稱擁有95%純度的綠茶提取物，Taiyo International則擁有90%以后純度,，兩家歐洲茶主要采購商在兒茶酚市場上雙足鼎立,。
英文原文：
Green Tea Slows Down Plaque Formation in Huntington's Disease - First Results in Model Organisms
Green tea can apparently inhibit the formation of the lethal protein aggregates that are a characteristic feature of Huntington's disease (HD). This finding was reported by Dagmar E. Ehrnhoefer, a member of the research group of Dr. Erich Wanker of the Max Delbrück Center for Molecular Medicine Berlin-Buch (MDC), Germany, at the international conference "Neurodegenerative Diseases: Molecular Mechanisms in a Functional Genomics Framework" in Berlin.
She was able to show in an in vitro experiment that the substance epigallocatechin-3-gallate (EGCG), extracted from green tea, interferes with very early events in the aggregation process of the mutant huntingtin protein. Cytoxicity is also reduced.
Moreover, the mobile function of transgenic flies carrying the Huntington's gene improved when they were fed the green tea substance.
The journal Human Molecular Genetics* has now published these research findings (Vol. 15, Nr. 18, 15. September 2006, pp. 2743-2751; advanced online access on August 7, 2006).
Dr. Wanker, who is also a professor at the Charité - Universitätsmedizin Berlin, and his colleagues hope that these findings can be a starting point for the development of a medical treatment for Huntington's disease and related diseases.
Huntington's disease, along with Alzheimer's and Parkinson's, belong to the family of neurodegenerative diseases caused by protein misfolding.
Jerky, uncontrolled movements, an unsteady gait and grimaces have given Huntington's disease (HD) its original common name that is still in use today: Huntington's chorea (Old Greek for "dance").
"Huntington's" in the name goes back to the American doctor George Huntington, who became the first to publish a detailed description of the disease in 1872.
The incurable disease is hereditary and has a prevalence of 1 in every 15,000 persons. In Germany, about 8,000 cases are currently known whereas in the US, 30,000 people have HD.
If a child inherits a mutated Huntington's gene from one affected parent, the disease inevitably develops, usually between the ages of 30 and 50. As a result, the nerve cells progressively degenerate in the areas of the brain that control movement and that are involved in memory and emotions. Ten to 30 years after the onset of the disease, Huntington's chorea leads to death.
In 1993, scientists discovered the gene that encodes the protein huntingtin. A mutation in this protein causes the disease and results in the aggregation of the mutant huntingtin protein within the cell nuclei of brain neurons.
In 1997, Dr. Wanker was able to demonstrate that these deposits or aggregates consist of misfolded huntingtin molecules. In the protein factories of the nerve cells of people with Huntington's disease, too many glutamine building blocks have been inserted into the amino acid sequence of huntingtin.
Due to the elongated polyglutamine chains which are formed, the protein loses its normal structure and can no longer be disposed of. Scientists hypothesize that these protein aggregates are toxic to nerve cells.
According to the findings of Dagmar Ehrnhoefer and Dr. Wanker, however, the substance epigallocatechin-3-gallate (EGCG) extracted from green tea slows down this aggregation process.
The research group hopes that these findings will be the starting point for developing a novel drug treatment for HD and related diseases in which misfolded proteins occur.
At the four-day conference, which began in Berlin-Buch on September 6th, around 200 genome researchers and clinicians from Canada, Europe, Japan, and the US discuss the latest findings on neurodegenerative diseases achieved with the aid of gene and protein research.
The organizers of the conference under the umbrella of the National Genome Research Network (NGFN), which is sponsored by the German Federal Ministry for Education and Research, were the MDC, the Charité - University Medical School, and the University of Bonn.
