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HIV相关痴呆的发病机制研究进展 被引量：1

Advances in pathogenesis of HIV associated dementia
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摘要 HIV相关痴呆是AIDS指征性疾病之一,表现为运动和认知功能障碍。尸检发现皮质萎缩和广泛的神经元细胞丢失,其发病机制还不十分清楚。目前发现HIV蛋白Tat和gp120具有直接和间接的神经毒性。谷氨酸、NO、钙、氧化应激、凋亡和小胶质细胞都参与了HIV相关神经变性的致病过程。本文综述了HIV相关神经毒性致病理论的最新进展,展示了阻止神经丢失和运动/认知功能衰退的潜在治疗干预途径。 As an AIDS-defining illness, HIV are associated with dementia manifests motor and cognitive deficits. Gross postmortem inspection shows cortical atrophy and widespread neuronal loss. Complete understanding of HIV neurotoxicity has been elusive. Both direct and indirect toxic mechanisms have been implicated in the neurotoxicity of the HIV proteins, Tat and gp120. The glutamatergic system, nitric oxide, calcium, oxidative stress, apoptosis, and microglia have all been implicated in the pathogenesis of HIV-related neuronal degeneration. The aim of this review was to summarize the most recent work and provide an overview to the current theories of HIV-related neurotoxicity and potential avenues of therapeutic interventions to prevent the neuronal loss and motor/cognitive deficits previously described.
作者 张洪海 陈德喜
机构地区 首都医科大学附属北京佑安医院性病艾滋病实验室
出处 《中国病原生物学杂志》 CSCD 2009年第2期133-136,共4页 Journal of Pathogen Biology
基金 国家自然科学基金面上项目(No.30770742)
关键词 HIV相关痴呆 发病机制 综述 HIV associated dementia pathogenesis review
分类号 R373.9 [医药卫生—病原生物学]
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参考文献32

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同被引文献14

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中国病原生物学杂志
2009年 第2期

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