在长期COVID中认知功能障碍的分子机制:叙述性审查
Elena Popa1,2, Andrei Emilian Popa3, Mihaela Poroch1,2
1Faculty of Medicine, "Grigore T. Popa" University of Medicine and Pharmacy, 16 Universitatii Str., 700115 Iasi, Romania.
长期的COVID会通过神经炎症和血脑屏障问题引起认知功能障碍. 了解这些大脑变化是开发治疗持续长期COVID症状的关键.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 病理生理学 病理生理学
背景情况:
- 长期的COVID经常导致持续和致残的认知功能障碍.
- 这种神经认知障碍背后的精确分子机制尚未完全理解.
研究的目的:
- 审查和综合有关将SARS-CoV-2感染与长期神经认知后果联系起来的病理生理机制的现有证据.
- 突出潜在的治疗目标和进一步研究的需要.
主要方法:
- 现有科学文献的叙述性审查.
- 综合关于神经炎症,血脑屏障破坏,免疫失调和神经内分泌失衡的证据.
主要成果:
- 关键机制包括微质激活,细胞因子释放 (IL-6,TNF-α),炎症酶激活 (NLRP3) 和血管异常.
- 血脑屏障的破坏,内皮功能障碍和下丘脑-垂体-上腺轴功能障碍有助于神经炎症和认知症状.
- 生物标志物 (GFAP,NFL,IL-6,S100B) 和与阿尔茨海默病重叠的转录基因特征 (tau失调,氧化应激,质反应) 被确定.
结论:
- 持续的神经炎症,BBB干扰和免疫失调是长期COVID认知功能障碍的核心.
- 了解这些分子通路对于开发向疗法和识别有风险的个体至关重要.
- 需要进行纵向研究和综合生物标志物分析,才能充分阐明长期COVID中认知障碍的轨迹.
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