Advanced Maillard reaction end products, free radicals, and protein oxidation in Alzheimer's disease.
Advanced Maillard reaction end products, free radicals, and protein oxidation in Alzheimer's disease.
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阿尔茨海默病中的高级美拉德反应终产物、自由基和蛋白质氧化。
DOI：
10.1111/j.1749-6632.1994.tb21836.x
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发表时间：
1994
影响因子：
5.2
通讯作者：
Perry,G
中科院分区：
文献类型：
--
作者：
Smith,MA;Richey,PL;Taneda,S;Kutty,RK;Sayre,LM;Monnier,VM;Perry,G
越来越多的证据表明，自由基的产生和氧化应激参与阿尔茨海默病的发病机制。我们的实验室最近发现了两个高级糖基化终产物与阿尔茨海默病的病理性神经元缠结和老年斑有关。已知这些糖基化相关的翻译后修饰在氧化应激期间启动和增强。此外，我们还证明了血红素加氧酶-1，一种在氧化应激过程中诱导的酶，参与抗氧化分子的产生，与病理损伤密切相关;在对照组大脑中几乎完全不存在。我们提出的证据表明，阿尔茨海默病的精液特征，包括淀粉样蛋白-P沉积，神经元缠结的形成，特定神经元群体的变性，并且病理损伤在体内的持续性和它们在体外的相对不溶性都可能与特定的氧化应激型机制有关。
Evidence that free-radical production and oxidative stress are involved in the pathogenesis of Alzheimer disease is increasing. Our laboratory recently found two advanced glycosylation end products associated with the pathological neurofibrillary tangles and senile plaques of Alzheimer’s disease. These glycation-related posttranslational modifications are known to be initiated and potentiated during periods of oxidative stress. Further, we have also demonstrated that heme oxygenase-1, an enzyme induced during oxidative stress and involved in the production of antioxidant molecules, is found in close association with the pathological lesions; being almost completely absent in control brains.We present evidence that the seminal features of Alzheimer’s disease, including amyloid-P deposition, neurofibrillary tangle formation, degeneration of specific neuronal populations, and the persistence of the pathological lesions in vivo and their relative insolubility in vitro may all be related to specific oxidative stress-type mechanisms.