Alzheimer disease: evidence for a central pathogenic role of iron-mediated reactive oxygen species.
Alzheimer disease: evidence for a central pathogenic role of iron-mediated reactive oxygen species.
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DOI：
10.3233/jad-2004-6208
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发表时间：
2004
期刊：
影响因子：
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通讯作者：
G. Casadesus;Mark A. Smith;Xiongwei Zhu;G. Aliev;A. D. Cash;K. Honda;R. Petersen;George Perry
中科院分区：
文献类型：
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作者：
G. Casadesus;Mark A. Smith;Xiongwei Zhu;G. Aliev;A. D. Cash;K. Honda;R. Petersen;George Perry
自由基的形成、铁和铜的分布异常以及金属催化的氧化都在阿尔茨海默病中被注意到，并且被认为在疾病发病机制中发挥着重要作用。金属催化的羟基自由基形成会对阿尔茨海默病中脆弱神经元群体中发现的每一类大分子造成损害。事实上，氧化还原活性存在于脆弱神经元的细胞质中。由于氧化损伤代表阿尔茨海默病最早的病理变化之一，因此异常的氧化还原活性很可能是向疾病状态转变的最早变化之一。在这篇综述中，我们考虑了大量的证据，表明金属在阿尔茨海默病中发挥着核心作用。
Free radical formation, abnormalities in iron and copper distribution, and metal-catalyzed oxidation have all been noted in Alzheimer disease and are thought to play an important role in disease pathogenesis. Metal-catalyzed hydroxyl radical formation results in damage to every category of macromolecule found in the vulnerable neuronal populations in Alzheimer disease. In fact, redox activity resides within the cytosol of vulnerable neurons. Since oxidative damage represents one of the earliest pathological changes in Alzheimer disease, it is likely that aberrant redox activity is among the earliest changes in the transition to the disease state. In this review, we consider the wealth of evidence implicating a central role for metals in Alzheimer disease.