长期的COVID作为一种tauopathy: "脑雾"和"融合风暴"的"脑雾"
Adonis Sfera1,2,3, Leah Rahman4, Carlos Manuel Zapata-Martín Del Campo5
1Paton State Hospital, 3102 Highland Ave, Patton, CA 92369, USA.
International journal of molecular sciences
|August 26, 2023
概括
长期COVID,或SARS-CoV-2的后急性后续,由于慢性炎症和病毒残留,导致持续的"脑雾". 这种观点探讨了病原遗传机制,潜在的生物标志物,如微生物DNA和酸化,以及诸如神经刺激等治疗方法.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 病毒学 病毒学
背景情况:
- 长期COVID呈现持续症状,特别是认知障碍 ("脑雾"),影响生活质量和医疗保健成本.
- 导致SARS-CoV-2引起的认知缺陷的确切原因仍然难以捉摸,主要假设是病毒储库的慢性炎症.
- 病毒在衰老细胞 (包括微质细胞和星球细胞) 中的持续存在可能导致神经毒性表型,并导致认知功能障碍.
研究的目的:
- 检查长期COVID认知障碍背后的病原遗传机制.
- 确定长期COVID的潜在生物标志物,包括微生物无细胞DNA,介质素22和酸化.
- 讨论通过皮肤进行神经刺激的潜在治疗益处.
主要方法:
- 审查有关SARS-CoV-2病原和长期COVID症状的现有文献.
- 假设病毒机制涉及细胞融合 (合成细胞形成) 和宿主细胞衰老.
- 探索肠-大脑轴和微生物转位在神经炎症中的作用.
主要成果:
- 病毒原体可能会诱导结合细胞,促进的过酸化和认知缺陷.
- 过早的内皮衰老可能会增加屏障的透性,允许微生物成分到达大脑.
- 转移的微生物产品,如脂多糖类,可能会触发Tau过酸化,导致记忆问题.
结论:
- 由病毒储存和细胞融合驱动的慢性炎症可能是导致长期COVID认知障碍的原因.
- 微生物无细胞DNA,IL-22和化Tau是诊断和监测的潜在生物标志物.
- 通过皮肤进行的神经刺激显示出作为治疗长期COVID症状的治疗干预的前景.
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