Recent Advances in the Molecular and Cellular Mechanisms of gp120-Mediated Neurotoxicity.

Recent Advances in the Molecular and Cellular Mechanisms of gp120-Mediated Neurotoxicity.
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DOI:
10.3390/cells11101599
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发表时间:
2022-05-10
期刊:
影响因子:
6
通讯作者:
--
中科院分区:
生物学2区
文献类型:
--
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人类免疫缺陷病毒(HIV)感染者的不同大脑区域经常出现轴突变性和突触丢失。然而,考虑到HIV不感染神经元,在这些个体中观察到的病理学改变的根本原因尚不清楚。实验数据表明,病毒蛋白,包括包膜蛋白gp 120,导致突触病理,随后神经元细胞死亡。这些对突触的神经毒性作用可能是各种降低突触可塑性的机制的结果。在本文中,我们将简要介绍新出现的概念与gp 120的能力,以促进突触的退化,无论是直接损害轴突细胞骨架和/或间接激活树突中的p75神经营养因子受体死亡结构域。
Axonal degeneration and loss of synapses are often seen in different brain areas of people living with human immunodeficiency virus (HIV). Nevertheless, the underlying causes of the pathological alterations observed in these individuals are poorly comprehended, considering that HIV does not infect neurons. Experimental data have shown that viral proteins, including the envelope protein gp120, cause synaptic pathology followed by neuronal cell death. These neurotoxic effects on synapses could be the result of a variety of mechanisms that decrease synaptic plasticity. In this paper, we will briefly present new emerging concepts connected with the ability of gp120 to promote the degeneration of synapses by either directly damaging the axonal cytoskeleton and/or the indirect activation of the p75 neurotrophin receptor death domain in dendrites.
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