The neurobiology of isoprostanes and Alzheimer's disease

被引：52

作者：

Pratico, Domenico ^{[1
]}

机构：

[1] Temple Univ, Sch Med, Dept Pharmacol, Philadelphia, PA 19140 USA

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS | 2010年 / 1801卷 / 08期

关键词：

Isoprostane; Oxidative stress; Alzheimer's disease; Amyloid beta; Thromboxane receptor; APOLIPOPROTEIN-E-DEFICIENT; REDUCES OXIDATIVE DAMAGE; LIPID-PEROXIDATION; THROMBOXANE RECEPTOR; AMYLOID PATHOLOGY; BRAIN; STRESS; F-2-ISOPROSTANES; MODEL; ACTIVATION;

D O I：

10.1016/j.bbalip.2010.01.009

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

In its sporadic form Alzheimer's disease (AD) results from a combination of genetic and environmental risk factors with abnormal oxidative reactions, which result in free radical mediated injury of the brain. Isoprostanes are oxidized lipids formed by a free radical mediated mechanism, which in recent years have emerged as a reliable and sensitive marker of lipid peroxidation and oxidative stress. Consistent data show that they are increased in the brain of human AD as well as AD animal models. Besides their role as biomarkers, isoprostanes possess important biological effects, functioning as mediators of the cellular response to oxidative stress within the CNS. Recent evidence indicates that these lipid oxidation products, by activating the thromboxane receptor system, mediate the pro-amyloidotic neuronal response to oxidative stress in an experimental model of AD. This novel observation has important clinical implication, since pharmacologic modulation of the TP receptor system by selective antagonists, some of which are already available, could represent a novel therapeutic opportunity for AD as disease-modifying agents. (C) 2010 Elsevier B.V. All rights reserved.

引用

页码：930 / 933

页数：4

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