In search of the neuroprotective mechanism of thiazolidinediones in Parkinson's disease

被引：16

作者：

Ridder, Dirk A. ^{[1
]}

Schwaninger, Markus ^{[1
]}

机构：

[1] Univ Lubeck, Inst Expt & Clin Pharmacol & Toxicol, D-23538 Lubeck, Germany

来源：

EXPERIMENTAL NEUROLOGY | 2012年 / 238卷 / 02期

关键词：

MPTP; MPP+; Glitazones; Oxidative stress; PPAR gamma; ACTIVATED-RECEPTOR-GAMMA; NF-KAPPA-B; CENTRAL-NERVOUS-SYSTEM; PROGRAMMED CELL-DEATH; PPAR-GAMMA; MOUSE MODEL; AGONIST PIOGLITAZONE; ALZHEIMERS-DISEASE; MITOCHONDRIAL DYSFUNCTION; INFLAMMATORY RESPONSE;

D O I：

10.1016/j.expneurol.2012.08.012

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The oral antidiabetic thiazolidinediones exert protective effects in models of Parkinson's disease and other neurological diseases. While the antidiabetic effect is due to activation of PPAR gamma, the mechanisms underlying the neuroprotection are more controversial. It may involve activation of PPAR gamma blocking inflammation and apoptosis. However, new evidence suggests an antioxidative PPAR gamma-independent action. Here we discuss recent data on the mode of action of TZDs in models of PD and their implication for the translation into the clinic. (C) 2012 Elsevier Inc. All rights reserved.

引用

页码：133 / 137

页数：5