Wallace David R
Department of Pharmacology and Physiology and Department of Forensic Sciences, Center for Health Sciences, Oklahoma State University, Tulsa, OK 74107-1898, USA.
J Biomed Biotechnol. 2006;2006(3):65741. doi: 10.1155/JBB/2006/65741.
Individuals suffering from human immunodeficiency virus type 1 (HIV-1) infection suffer from a wide range of neurological deficits. The most pronounced are the motor and cognitive deficits observed in many patients in the latter stages of HIV infection. Gross postmortem inspection shows cortical atrophy and widespread neuronal loss. One of the more debilitating of the HIV-related syndromes is AIDS-related dementia, or HAD. 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 is 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.
感染1型人类免疫缺陷病毒（HIV-1）的个体存在广泛的神经功能缺损。最明显的是在HIV感染后期许多患者中观察到的运动和认知缺陷。大体尸检显示皮质萎缩和广泛的神经元丧失。与HIV相关的综合征中更具致残性的一种是艾滋病相关痴呆症（HAD）。对HIV神经毒性的全面理解一直难以实现。直接和间接毒性机制都与HIV蛋白Tat和gp120的神经毒性有关。谷氨酸能系统、一氧化氮、钙、氧化应激、细胞凋亡和小胶质细胞都与HIV相关神经元变性的发病机制有关。本综述的目的是总结最新研究工作，并概述当前关于HIV相关神经毒性的理论以及预防先前所述神经元丧失和运动/认知缺陷的潜在治疗干预途径。
