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SARS-CoV-2 阻碍了来自 iPSC 的多巴胺基神经元中多巴胺的产生

G Cappelletti¹, E V Carsana², G Lunghi²

¹Department of Biomedical and Clinical Sciences, University of Milan, via G.B. Grassi 74, 20157 Milan, Italy.

Experimental and molecular pathology

|September 29, 2023

概括

后COVID条件可能涉及由于SARS-CoV-2影响多巴胺通路的神经症状. 研究表明,欧盟和三角洲变种降低神经元中的多巴胺,影响神经功能.

科学领域:

神经科学是一个神经科学.
病毒学病毒学
分子生物学分子生物学

背景情况:

在COVID-19 (后COVID) 后,人们越来越多地认识到长期症状.
神经学表现很常见,促使人们对潜在机制进行调查.
假设SARS-CoV-2和多巴胺通路之间存在潜在联系,但尚未得到科学证据.

研究的目的:

为了研究SARS-CoV-2感染对多巴胺能神经元的影响.
为了确定不同的SARS-CoV-2变种是否会影响多巴胺代谢.
在COVID后的条件下探索病毒感染和神经症状之间的关系.

主要方法:

人类诱导多能干细胞 (iPSC) 衍生的多巴胺基神经元感染EU,Delta和Omicron SARS-CoV-2变种.
细胞内和细胞外多巴胺水平的量化.
对关键多巴胺合成和运输基因 (tyrosine hydroxylase,DOPA-decarboxylase,多巴胺载体) 的mRNA和蛋白质表达的分析.
评估神经元压力标志物和MAP2和TAU蛋白的表达.

主要成果:

感染欧盟和三角形SARS-CoV-2变种,但不是Omicron,显著降低了神经元中的多巴胺水平.
氨酸氧酶mRNA的调节升高,但其蛋白质水平下降.
在mRNA和蛋白质水平上,DOPA-脱碳酶和多巴胺载体显示下调.
感染SARS-CoV-2导致MAP2和TAU表达发生变化,神经元压力标志物增加.

结论:

SARS-CoV-2 感染,特别是在欧盟和三角洲变种中,会破坏多巴胺代谢和多巴胺神经元中的多巴胺生成.
这些发现为在后COVID条件下观察到的神经症状提供了潜在的分子解释.
这项研究强调了SARS-CoV-2的神经生物学影响,并表明特定变体可能对神经元功能产生差异性影响.

关键词:

多巴胺是一种多巴胺.多巴氨基神经元是多巴氨基神经元.神经应激是一种神经应激.在COVID后,我们将继续努力.这是一种SARS-CoV-2感染.在SARS-CoV-2变种中.

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