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在COVID-19后的低血中,嗅觉通路中没有表现出主要的神经退行性标记物
Tommaso Schirinzi1, Daniela Maftei2, Riccardo Maurizi3
1Unit of Neurology, Department of Systems Medicine, Tor Vergata University of Rome, Via Montpellier 1, 00133, Rome, Italy. t.schirinzi@yahoo.com.
Molecular neurobiology
|April 3, 2024
概括
持续的COVID-19后嗅觉丧失 (低湿症) 可能不是来自嗅觉神经元的神经退行. 早期分析没有发现这些细胞中存在关键阿尔茨海默氏症或帕金森病标志物的证据.
科学领域:
- 神经科学是一个神经科学.
- 病理学 病理学 病理学
- 耳鼻喉科 耳鼻喉科 耳鼻喉科
背景情况:
- 持续的COVID-19后嗅觉障碍 (低湿症) 有一个不清楚的生物学基础.
- 嗅觉功能障碍可能是神经退行性疾病的早期症状,表明潜在的中枢嗅觉回路参与.
- 嗅觉神经元 (ONs) 可以反映大脑病理,为分子事件提供一个窗口.
研究的目的:
- 为了研究持续的COVID-19后嗅觉损失患者的嗅觉神经元,寻找神经退行症的迹象.
- 分析ONs对α-synuclein,β-amyloid,tau病理,轴突损伤和线粒体功能障碍的标志物.
主要方法:
- 通过非侵入性刷毛收集了10名COVID-19后持续性低血 (>6个月) 的患者和10名对照者的嗅觉神经元.
- 使用免疫光染色来定量蛋白质.
- 使用RT-PCR用于对特定病理标记物的基因表达分析.
主要成果:
- 在患者和对照组之间,在ONs水平的寡合性α-synuclein,粉样β或tau蛋白中没有发现显著差异.
- 神经纤维光链 (NfL),细胞染色体C氧化酶亚单元3 (COX3) 和热冲击蛋白60 (HSP60) 的水平也相似.
- 结果表明,在COVID-19后早期的低血中,没有证据表明有同核病变,粉样β代谢问题,神经元损伤或线粒体功能障碍.
结论:
- 持续性COVID-19后低血的早期阶段似乎不是由同核蛋白病变,粉样蛋白-β病理或嗅觉系统内的显著神经元损伤驱动的.
- 需要进一步的研究,以阐明COVID-19感染后持续的气味丧失背后的精确机制.
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