The translocator protein as a drug target in Alzheimer's disease

被引：19

作者：

Chua, Sook W. ^{[1
,2
]}

Kassiou, Michael ^{[2
,3
,4
]}

Ittner, Lars M. ^{[1
,5
]}

机构：

[1] Univ New S Wales, Sch Med Sci, Dementia Res Unit, Sydney, NSW 2052, Australia

[2] Brain & Mind Res Inst, Sydney, NSW 2050, Australia

[3] Univ Sydney, Sch Chem, Sydney, NSW 2006, Australia

[4] Univ Sydney, Discipline Med Radiat Sci, Sydney, NSW 2006, Australia

[5] Neurosci Res Australia, Sydney, NSW 2052, Australia

来源：

EXPERT REVIEW OF NEUROTHERAPEUTICS | 2014年 / 14卷 / 04期

基金：

澳大利亚研究理事会; 英国医学研究理事会;

关键词：

translocator protein; neuroinflammation; drug development; positron emission topography; microglia; Alzheimer's disease; TSPO; PERIPHERAL BENZODIAZEPINE-RECEPTOR; DIAZEPAM-BINDING INHIBITOR; VIVO RADIOLIGAND BINDING; H-3; PK; 11195; 18 KDA TSPO; IN-VIVO; MICROGLIAL ACTIVATION; HIGH-AFFINITY; AMYLOID-BETA; HUMAN BRAIN;

D O I：

10.1586/14737175.2014.896201

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

The translocator protein (TSPO) recently emerged as a potential drug target in Alzheimer's disease (AD). This has been fuelled mainly by positron emission topography studies that show the upregulation of TSPO in AD, especially in relation to microgliosis and astrogliosis in amyloid-beta and tau pathology. Although data as to the exact role of TSPO in AD is still inconclusive, TSPO appears to be involved in neuroinflammatory processes and AD has been shown to involve substantial inflammation. Therefore, further development and investigation of the pharmacological effect of TSPO ligands in AD pathology are warranted.

引用

页码：439 / 448

页数：10

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