Elevation of glutathione as a therapeutic strategy in Alzheimer disease

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• 作者：Chava B. Pocernich^a ; ^b ; D. Allan Butterfield^a ; ^b ; ^c ; ^{dabcns@uky.edu}
• 关键词：Alzheimer disease (AD) ; Mild cognitive impairment (MCI) ; Amyloid 尾-peptide ; Glutathione (GSH) ; N-acetylcysteine (NAC) ; 纬-Glutamylcysteine ethyl ester
• 刊名：Biochimica et Biophysica Acta (BBA)/Molecular Basis of Disease
• 出版年：2012
• 期刊代码：19_09254439
• 类别：bio
• 出版时间：May, 2012
• 卷：1822
• 期：5
• 页码：625-630
• 文件大小：471 K

摘要

Oxidative stress has been associated with the onset and progression of mild cognitive impairment (MCI) and Alzheimer disease (AD). AD and MCI brain and plasma display extensive oxidative stress as indexed by protein oxidation, lipid peroxidation, free radical formation, DNA oxidation, and decreased antioxidants. The most abundant endogenous antioxidant, glutathione, plays a significant role in combating oxidative stress. The ratio of oxidized to reduced glutathione is utilized as a measure of intensity of oxidative stress. Antioxidants have long been considered as an approach to slow down AD progression. In this review, we focus on the elevation on glutathione through N-acetyl-cysteine (NAC) and 纬-glutamylcysteine ethyl ester (GCEE) as a potential therapeutic approach for Alzheimer disease. This article is part of a Special Issue entitled: Antioxidants and Antioxidant Treatment in Disease.