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甲基乙二醛在阿尔茨海默病中的作用。

Role of methylglyoxal in Alzheimer's disease.

作者信息

Angeloni Cristina, Zambonin Laura, Hrelia Silvana

机构信息

Department for Life Quality Studies, Alma Mater Studiorum, University of Bologna, Corso d'Augusto 237, 47900 Rimini, Italy.

Department of Pharmacy and Biotechnology, Alma Mater Studiorum, University of Bologna, Via Irnerio 48, 40126 Bologna, Italy.

出版信息

Biomed Res Int. 2014;2014:238485. doi: 10.1155/2014/238485. Epub 2014 Mar 9.

DOI:10.1155/2014/238485
PMID:24734229
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3966409/
Abstract

Alzheimer's disease is the most common and lethal neurodegenerative disorder. The major hallmarks of Alzheimer's disease are extracellular aggregation of amyloid β peptides and, the presence of intracellular neurofibrillary tangles formed by precipitation/aggregation of hyperphosphorylated tau protein. The etiology of Alzheimer's disease is multifactorial and a full understanding of its pathogenesis remains elusive. Some years ago, it has been suggested that glycation may contribute to both extensive protein cross-linking and oxidative stress in Alzheimer's disease. Glycation is an endogenous process that leads to the production of a class of compounds known as advanced glycation end products (AGEs). Interestingly, increased levels of AGEs have been observed in brains of Alzheimer's disease patients. Methylglyoxal, a reactive intermediate of cellular metabolism, is the most potent precursor of AGEs and is strictly correlated with an increase of oxidative stress in Alzheimer's disease. Many studies are showing that methylglyoxal and methylglyoxal-derived AGEs play a key role in the etiopathogenesis of Alzheimer's disease.

摘要

阿尔茨海默病是最常见且致命的神经退行性疾病。阿尔茨海默病的主要特征是β淀粉样肽的细胞外聚集,以及由过度磷酸化的tau蛋白沉淀/聚集形成的细胞内神经原纤维缠结。阿尔茨海默病的病因是多因素的,对其发病机制的全面理解仍然难以捉摸。几年前,有人提出糖基化可能导致阿尔茨海默病中广泛的蛋白质交联和氧化应激。糖基化是一个内源性过程,会导致一类称为晚期糖基化终产物(AGEs)的化合物的产生。有趣的是,在阿尔茨海默病患者的大脑中观察到AGEs水平升高。甲基乙二醛是细胞代谢的一种反应性中间体,是AGEs最有效的前体,并且与阿尔茨海默病中氧化应激的增加密切相关。许多研究表明,甲基乙二醛和甲基乙二醛衍生的AGEs在阿尔茨海默病的病因发病机制中起关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f32/3966409/78da60c5936f/BMRI2014-238485.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f32/3966409/431fabbb5026/BMRI2014-238485.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f32/3966409/78da60c5936f/BMRI2014-238485.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f32/3966409/431fabbb5026/BMRI2014-238485.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f32/3966409/78da60c5936f/BMRI2014-238485.002.jpg

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