Redox Proteomics in Some Age-Related Neurodegenerative Disorders or Models Thereof

被引:6
|
作者
Butterfield D.A. [1 ,2 ]
Abdul H.M. [1 ,2 ]
Newman S. [1 ,2 ]
Reed T. [1 ,2 ]
机构
[1] Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY
[2] Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY
来源
NeuroRX | 2006年 / 3卷 / 3期
基金
美国国家卫生研究院;
关键词
(1-42); Aβ; AD; Alzheimer's disease; amyloid beta-peptide; mass spectrometry; protein oxidation; Redox proteomics;
D O I
10.1016/j.nurx.2006.05.003
中图分类号
学科分类号
摘要
Summary: Neurodegenerative diseases cause memory loss and cognitive impairment. Results from basic and clinical scientific research suggest a complex network of mechanisms involved in the process of neurodegeneration. Progress in treatment of such disorders requires researchers to better understand the functions of proteins involved in neurodegenerative diseases, to characterize their role in pathogenic disease mechanisms, and to explore their roles in the diagnosis, treatment, and prevention of neurodegenerative diseases. A variety of conditions of neurodegenerative diseases often lead to post-translational modifications of proteins, including oxidation and nitration, which might be involved in the pathogenesis of neurodegenerative diseases. Redox proteomics, a subset of proteomics, has made possible the identification of specifically oxidized proteins in neurodegenerative disorders, providing insight into a multitude of pathways that govern behavior and cognition and the response of the nervous system to injury and disease. Proteomic analyses are particularly suitable to elucidate post-translational modifications, expression levels, and protein-protein interactions of thousands of proteins at a time. Complementing the valuable information generated through the integrative knowledge of protein expression and function should enable the development of more efficient diagnostic tools and therapeutic modalities. Here we review redox proteomic studies of some neurodegenerative diseases. © 2006 The American Society for Experimental NeuroTherapeutics, Inc.
引用
收藏
页码:344 / 357
页数:13
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