Sultana Rukhsana, Perluigi Marzia, Butterfield D Allan
Department of Chemistry, and Sanders-Brown Center on Aging, University of Kentucky, Lexington, Kentucky 40506-0055, USA.
Antioxid Redox Signal. 2006 Nov-Dec;8(11-12):2021-37. doi: 10.1089/ars.2006.8.2021.
Alzheimer's disease (AD), the leading cause of dementia, involves regionalized neuronal death, synaptic loss, and an accumulation of intraneuronal, neurofibrillary tangles and extracellular senile plaques. Although the initiating causes leading to AD are unknown, a number of previous studies reported the role of oxidative stress in AD brain. Postmortem analysis of AD brain showed elevated markers of oxidative stress including protein nitrotyrosine, carbonyls in proteins, lipid oxidation products, and oxidized DNA bases. In this review, we focus our attention on the role of protein oxidation and lipid peroxidation in the pathogenesis of AD. Particular attention is given to the current knowledge about the redox proteomics identification of oxidatively modified proteins in AD brain.
阿尔茨海默病（AD）是痴呆的主要病因，涉及区域性神经元死亡、突触丧失以及神经元内神经原纤维缠结和细胞外老年斑的积累。尽管导致AD的起始原因尚不清楚，但此前的一些研究报道了氧化应激在AD大脑中的作用。对AD大脑的尸检分析显示氧化应激标志物升高，包括蛋白质硝基酪氨酸、蛋白质中的羰基、脂质氧化产物和氧化的DNA碱基。在本综述中，我们将注意力集中在蛋白质氧化和脂质过氧化在AD发病机制中的作用。特别关注目前关于AD大脑中氧化修饰蛋白质的氧化还原蛋白质组学鉴定的知识。
