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首页> 美国卫生研究院文献>other >Implementing Neuronal plasticity in NeuroAIDS: The Experience of Brain-derived Neurotrophic Factor and Other Neurotrophic Factors
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Implementing Neuronal plasticity in NeuroAIDS: The Experience of Brain-derived Neurotrophic Factor and Other Neurotrophic Factors

机译：在NeuroAIDS中实现神经元可塑性：脑源性神经营养因子和其他神经营养因子的经验

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Human immunodeficiency virus type-1 (HIV) causes mild or severe neurological problems, termed HIV-associated neurocognitive disorder (HAND), even when HIV patients receive antiretroviral therapy. Thus, novel adjunctive therapies are necessary to reduce or abolish the neurotoxic effect of HIV. However, new therapies require a better understanding of the molecular and cellular mechanisms of HIV-induced neurotoxicity. HAND subjects are characterized by being profoundly depressed, and they experience deficits in memory, learning and movements. Experimental evidence has also shown that HIV reduces neurogenesis. These deficits resemble those occurring in premature brain aging or in a brain with impaired neural repair properties. Thus, it appears that HIV diminishes neuronal survival, along with reduced neuronal connections. These two phenomena should not occur in the adult and developing brain when synaptic plasticity is promoted by neurotrophic factors, polypeptides that are present in adult synapses. This review will outline experimental evidence as well as present emerging concepts for the use of neurotrophic factors and in particular brain-derived neurotrophic factor as an adjunct therapy to prevent HIV-mediated neuronal degeneration and restore the loss of synaptic connections.
机译：1型人类免疫缺陷病毒（HIV）会导致轻度或重度神经系统问题，称为HIV相关神经认知障碍（HAND），即使HIV患者接受抗逆转录病毒治疗也是如此。因此，新颖的辅助疗法对于减少或消除HIV的神经毒性作用是必要的。但是，新疗法需要更好地了解HIV诱导的神经毒性的分子和细胞机制。手科的特征是情绪低落，他们的记忆力，学习能力和运动能力都较弱。实验证据还表明，艾滋病毒可减少神经发生。这些缺陷类似于大脑过早衰老或神经修复特性受损的大脑中的缺陷。因此，似乎HIV减少了神经元的存活，同时减少了神经元的连接。当神经营养因子（存在于成人突触中的多肽）促进突触可塑性时，这两种现象不应在成人和发育中的大脑中发生。这篇综述将概述实验证据，以及有关使用神经营养因子，尤其是脑源性神经营养因子作为预防HIV介导的神经元变性并恢复突触连接丧失的辅助疗法的新兴概念。

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