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哥伦比亚研究者发现一种酶治疗患有Alzheimer的大
Boosting a newly discovered enzyme helps mice regain normal cognitive function
NEW YORK August 24, 2006 -- Researchers at Columbia University Medical Center have successfully restored normal memory and synaptic function in mice suffering from Alzheimer's disease. The study was published today on the website of the journal Cell.
哥伦比亚研究者成功修复了患有Alzheimer大鼠的记忆。最新发现一种酶可以帮助大鼠恢复一般的认知功能。2006.08.24美国—哥伦比亚大学医学部的研究者已经成功的恢复了患有Alzheimer大鼠的正常的记忆和突触功能。论文已经发表在今天的细胞学杂志的网站上。
Scientists at Columbia's Taub Institute for Research on Alzheimer's Disease and the
Aging Brain have identified an enzyme that is required for normal cognition but that is impaired in a mouse model of Alzheimer's. They discovered that mice regained the ability to form new memories when the enzyme's function was elevated.
哥伦比亚 Taub研究所研究Alzheimer疾病和老年病的研究者已经辨认出一种维持正常的认知功能的一种酶，在Alzheimer大鼠模型中已经被成功的修复了。当酶开始起效的时候，他们发现大鼠重新获得了形成新记忆的能力
The research suggests that boosting the function of this enzyme, known as ubiquitin C-terminal hydrolase L1 (Uch-L1), may provide a promising strategy for battling Alzheimer's disease, and perhaps reversing its effects.
研究者发现这种酶的主要功效，如泛激素，c羟基末端水解酶L1，可能产生对抗Alzheimer的有效的物质，并且逆转它的疗效。
In the new study, the Columbia researchers discovered that the enzyme Uch-L1 is part of a molecular network that controls a memory molecule called CREB, which is inhibited by amyloid beta proteins in people with Alzheimer's. By increasing Uch-L1 levels in mice that had Alzheimer's, they were able to improve the animals' ability to create new memories.
最新的研究发现，哥伦比亚研究者发现水解酶L1是控制记忆的分子结构CREB的构成成分之一，被Alzheimer患者体内的淀粉样beta蛋白所抑制。提高患有Alzheimer大鼠水解酶L1的水平，能够提高大鼠形成新记忆的能力
"Because the amyloid beta proteins that cause Alzheimer's may play a normal, important physiological role in the body, we can't destroy them as a therapy," explained Ottavio Arancio, M.D., Ph.D., Assistant Professor of Pathology at Columbia University Medical Center and co-principal investigator of the study with Michael Shelanski, MD, Ph.D., Chairman of the Department of Pathology at the Columbia University College of Physicians and Surgeons. "What makes this newly discovered enzyme exciting as a potentially effective therapy is that it restores memory without destroying amyloid beta proteins."
因为淀粉样beta蛋白导致Alzheimer在体内主要起一个正常的、生理的作用，我们不能作为一个治疗手段来破坏它，Ottavio Arancio 哥伦比亚大学医学部教授助理和共同研究者Michael Shelanski 哥伦比亚大学外科病理部的主席说，值得兴奋的是，这种新发现的酶在没有破坏淀粉样beta蛋白的前提下，可以修复记忆。
The researchers tested the memory of the mice by putting them in a cage where they were exposed to a mild stimulus when they touched the cage floor. Mice with normal memory remain still the second time they're placed in the cage, as they recognize the place where they were initially exposed to the stimulus. But mice with Alzheimer's-like changes do not remember the place, and continue moving within the cage. When the Alzheimer's mice were treated with Uch-L1, they acted like normal mice, and remained still.
研究者试验大鼠的记忆，将他们放在一个笼子里，当他们接触到笼子底部的时候暴露在一个轻微的刺激物。正常记忆的大鼠当再次被放入笼子的时候，保持安静，因为他们可以辨认出这是他们原来笼子。但是患有Alzheimer的大鼠，不能记住原来的位置，继续在笼子里移动。但是当Alzheimer大鼠接受水解酶L1治疗后，表现同正常的大鼠一样，保持安静。
"While this discovery is very promising, its proven effectiveness is limited to animal models and it will take some time before it could lead to therapies in humans," said Dr. Shelanski. "We continue to work towards that crucial goal." The work was supported by the National Institutes of Neurological Disease and Stroke and the
Alzheimer's Center Program of the National Institute of Aging.
虽然这项发现非常有希望，但是实验仅是限于动物，人类接受治疗还需要一段时间。Shelanski说，我们将向着治疗的目标继续努力。这项研究由国立神经病及中风研究所和国际老年病协会Alzheimer中心资助。
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作者:admin@医学,生命科学 2010-12-17 07:31
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