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探索朊病毒疾病中神经退行性变的机制。

Discovering the mechanisms of neurodegeneration in prion diseases.

作者信息

DeArmond Stephen J

机构信息

Department of Pathology, Institute for Neurodegenerative Diseases, University of California, San Francisco, 94143-0511, USA.

出版信息

Neurochem Res. 2004 Nov;29(11):1979-98. doi: 10.1007/s11064-004-6872-2.

Abstract

The purpose of my chapter in this issue of Neuroscience Reviews dedicated to Dr. Lawrence Eng is to summarize my contributions to understanding the mechanisms of neurodegeneration in prion diseases. I explain that I was able to advance the field of prion disease neuropathology largely because of the foundation of neurochemistry and immunohistochemistry that I learned while working 5 years in Dr. Eng's laboratory. In my review, I relate how my Neuropathology Research Laboratory began as a collaboration with Dr. Stanley Prusiner 20 years ago that led from immunohistochemical staining of amyloid plaques in rodent and human brains using prion protein-specific antibodies to molecular evidence that the abnormal prion protein, PrP(Sc), is the cause of the clinically relevant neuropathological changes in animal and human prion diseases.

摘要

在本期献给劳伦斯·恩格博士的《神经科学评论》中,我这一章的目的是总结我在理解朊病毒疾病神经退行性变机制方面所做的贡献。我解释说,我之所以能够推动朊病毒疾病神经病理学领域的发展,很大程度上是因为我在恩格博士的实验室工作5年期间所学的神经化学和免疫组织化学基础。在我的综述中,我讲述了我的神经病理学研究实验室是如何在20年前与斯坦利·普鲁西纳博士合作起步的,从使用朊病毒蛋白特异性抗体对啮齿动物和人类大脑中的淀粉样斑块进行免疫组织化学染色,到获得分子证据,证明异常朊病毒蛋白PrP(Sc)是动物和人类朊病毒疾病临床相关神经病理学变化的病因。

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