HIV-associated neurocognitive disorder: pathogenesis and therapeutic opportunities.
HIV-associated neurocognitive disorder: pathogenesis and therapeutic opportunities.
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DOI：
10.1007/s11481-010-9205-z
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发表时间：
2010-09
影响因子：
6.2
通讯作者：
Jordan-Sciutto, Kelly L.
中科院分区：
文献类型：
--
作者：
Lindl, Kathryn A.;Marks, David R.;Kolson, Dennis L.;Jordan-Sciutto, Kelly L.
关键词：
人类免疫缺陷病毒1型(HIV)感染目前影响着全球4000多万人，并与至少30%的感染者的中枢神经系统(CNS)中断有关。高效抗逆转录病毒疗法的使用减少了发病率，但并未降低较高认知和皮质功能轻度损害(艾滋病毒相关神经认知障碍)的患病率，并大幅减少了更严重形式的痴呆(艾滋病毒相关痴呆)。此外，改善神经学结果将需要针对艾滋病毒诱导的神经退化机制的新的辅助治疗。识别这样的分子和药理学靶点需要了解中枢神经系统中不可逆神经元损伤之前的事件，如神经毒素(HIV蛋白和细胞因子)的作用、离子通道特性的破坏、突触损伤和成年神经发生的丧失。通过考虑HIV神经发病的具体机制和后果，统一的神经保护方法可能会出现，使用一种量身定制的、组合的和非侵入性的方法。
Human immunodeficiency virus type 1 (HIV) infection presently affects more that 40 million people worldwide, and is associated with central nervous system (CNS) disruption in at least 30% of infected individuals. The use of highly active antiretroviral therapy has lessened the incidence, but not the prevalence of mild impairment of higher cognitive and cortical functions (HIV-associated neurocognitive disorders) as well as substantially reduced a more severe form dementia (HIV-associated dementia). Furthermore, improving neurological outcomes will require novel, adjunctive therapies that are targeted towards mechanisms of HIV-induced neurodegeneration. Identifying such molecular and pharmacological targets requires an understanding of the events preceding irreversible neuronal damage in the CNS, such as actions of neurotoxins (HIV proteins and cellular factors), disruption of ion channel properties, synaptic damage, and loss of adult neurogenesis. By considering the specific mechanisms and consequences of HIV neuropathogenesis, unified approaches for neuroprotection will likely emerge using a tailored, combined, and non-invasive approach.
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