Involvement of quinolinic acid in AIDS dementia complex

被引：105

作者：

Guillemin, GJ

Kerr, SJ

Brew, BJ ^{[1
]}

机构：

[1] St Vincents Hosp, Ctr Immunol, Sydney, NSW 2010, Australia

[2] St Vincents Hosp, Dept Neurol, Sydney, NSW 2010, Australia

[3] St Vincents Hosp, Dept HIV Med, Sydney, NSW 2010, Australia

[4] Univ New S Wales, Sch Med, Kensington, NSW 2033, Australia

[5] Natl Ctr HIV Epidemiol & Clin Res, Sydney, NSW, Australia

[6] HIV Netherlands Australia Thailand Res Collaborat, Bangkok, Thailand

来源：

NEUROTOXICITY RESEARCH | 2005年 / 7卷 / 1-2期

关键词：

quinolinic acid; kynurenine; kynurenic acid; HIV; AIDS; dementia; inflammatory brain disease; cytokines; chemokines; N-methyl-D-aspartate; macrophages; microglia;

D O I：

10.1007/BF03033781

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

Human immunodeficiency virus (HIV) infection is often complicated by the development of acquired immunodeficiency syndrome (AIDS) dementia complex (ADC). Quinolinic acid (QUIN) is an end product of tryptophan, metabolized through the kynurenine pathway (KP) that can act as an endogenous brain excitotoxin when produced and released by activated macrophages/microglia, the very cells that are prominent in the pathogenesis of ADC. This review examines QUIN's involvement in the features of ADC and its role in pathogenesis. We then synthesize these findings into a hypothetical model for the role played by QUIN in ADC, and discuss the implications of this model for ADC and other inflammatory brain diseases.

引用

页码：103 / 123

页数：21

共 282 条

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