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【medical-news】新研究指出了环境因素与帕金森氏

http://www.eurekalert.org/pub_releases/2007-04/tpi-nsl040407.php

Public release date: 5-Apr-2007

New studies link the environment to Parkinson's disease
Research will open new possibilities for intervention and prevention
Sunnyvale, CA ?April 5, 2007 ?The Parkinson's Institute today announced that new findings concerning the role of environmental factors in the development of Parkinson's disease will be reported at Asilomar (Pacific Grove, CA) as part of the final meeting of the Collaborative Centers for Parkinson's Disease Environmental Research (CCPDER). This collaborative research effort, sponsored by the National Institute of Environmental Health Sciences (NIEHS), brings together investigators from Emory University, the University of California Los Angeles and The Parkinson's Institute, which has served as the coordinating center for the study.

Highlights of the research include:

The role of pesticides (eg. Paraquat and Dieldrin) as potential risk factors for Parkinson's disease, a role suggested by both epidemiological statistics and laboratory evidence.

The threat of toxic agents to damage neurons by causing the accumulation of harmful proteins.

Intraneuronal protein aggregates as markers of Parkinson's pathology, based on work carried out at The Parkinson's Institute indicating that these aggregates could be formed as a consequence of toxic exposure.

The importance of targeting a specific protein, alpha-synuclein, in order to achieve neuroprotection in Parkinson's

The role of inflammation in the development of Parkinson's disease and the possibility that anti-inflammatory drugs could be beneficial to patients.

The possibility that nicotine may act as a neuroprotective agent.

"Our collaboration with Emory University and UCLA has allowed us to make great strives in identifying environmental factors involved in the development of Parkinson's disease," said Donato A. Di Monte, M.D., director of basic research at The Parkinson's Institute. "The findings that will be discussed at Asilomar will help us better understand the disease process, intervene earlier with neuroprotective treatment and work on preventive measures against Parkinson's disease risk factors." 本人认领此文。如在48小时内未能提交译文,其他战友可自由认领。 http://www.eurekalert.org/pub_releases/2007-04/tpi-nsl040407.php

Public release date: 5-Apr-2007
公开发行日期:2007年4月5日

New studies link the environment to Parkinson's disease
新的研究指出了环境因素与帕金森氏症之间的联系

Research will open new possibilities for intervention and prevention
Sunnyvale, CA ?April 5, 2007 ?The Parkinson's Institute today announced that new findings concerning the role of environmental factors in the development of Parkinson's disease will be reported at Asilomar (Pacific Grove, CA) as part of the final meeting of the Collaborative Centers for Parkinson's Disease Environmental Research (CCPDER). This collaborative research effort, sponsored by the National Institute of Environmental Health Sciences (NIEHS), brings together investigators from Emory University, the University of California Los Angeles and The Parkinson's Institute, which has served as the coordinating center for the study.
研究将打开新的干预和阻止的可能性
加利福亚州的桑尼维尔,2007年4月5日,帕金森研究所今天宣布了关于环境因素在帕金森氏症发展中的角色的新发现,并将作为CCPDER(帕金森病环境研究计划协作中心)的最后会议的一部分公布在Asilomar(加利福亚州的帕西菲克•格罗夫)上。这项协作研究工作由国家环境卫生科学研究所(NIEHS)发起,汇集了来自埃默里大学、加利福尼亚大学洛杉矶分校和帕金森研究所的研究者。他们将担任研究的协调中心。

Highlights of the research include:
研究重点包括:

The role of pesticides (eg. Paraquat and Dieldrin) as potential risk factors for Parkinson's disease, a role suggested by both epidemiological statistics and laboratory evidence.
农药(例如:百草枯、狄氏剂)作为一个潜在的危险因素在帕金森氏病中的作用——一个通过流行病统计学和实验室证据得到暗示的作用。

The threat of toxic agents to damage neurons by causing the accumulation of harmful proteins.
毒剂对破坏神经元的威胁通过有害蛋白质的积累引起。

Intraneuronal protein aggregates as markers of Parkinson's pathology, based on work carried out at The Parkinson's Institute indicating that these aggregates could be formed as a consequence of toxic exposure.
帕金森研究所进行的工作表明这种聚集能够形成毒素暴露的后果,因此认为神经细胞内蛋白的聚集作为帕金森病理的标记。

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作者:admin@医学,生命科学    2011-08-12 17:20
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