Involvement of quinolinic acid in AIDS dementia complex
Involvement of quinolinic acid in AIDS dementia complex
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DOI：
10.1007/bf03033781
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发表时间：
2005-01-01
影响因子：
3.7
通讯作者：
Brew, BJ
中科院分区：
文献类型：
--
作者：
Guillemin, GJ;Kerr, SJ;Brew, BJ
人类免疫缺陷病毒 (HIV) 感染常常因获得性免疫缺陷综合征 (AIDS) 痴呆症 (ADC) 的发展而变得复杂。喹啉酸 (QUIN) 是色氨酸的最终产物，通过犬尿氨酸途径 (KP) 代谢，当激活的巨噬细胞/小胶质细胞（在 ADC 发病机制中起重要作用的细胞）产生和释放时，可充当内源性脑兴奋毒素。本综述探讨了 QUIN 与 ADC 特征的关系及其在发病机制中的作用。然后，我们将这些发现综合为 QUIN 在 ADC 中所发挥作用的假设模型，并讨论该模型对 ADC 和其他炎症性脑疾病的影响。
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.