Health Sciences Unit, Laboratory of Neurobiology of Inflammatory and Metabolic Processes, Graduate Program in Health Sciences, University of South Santa Catarina, Tubarao, Brazil.
School of Nutrition Sciences, Faculty of Health Sciences, University of Ottawa, Ottawa, Ontario, Canada.
Neuroimmunomodulation. 2022;29(4):269-281. doi: 10.1159/000526653. Epub 2022 Nov 2.
Many coronavirus disease 2019 (COVID-19)-recovered patients report signs and symptoms and are experiencing neurological, psychiatric, and cognitive problems. However, the exact prevalence and outcome of cognitive sequelae is unclear. Even though the severe acute respiratory syndrome coronavirus 2 has target brain cells through binding to angiotensin-converting enzyme 2 (ACE2) receptor in acute infection, several studies indicate the absence of the virus in the brain of many COVID-19 patients who developed neurological disorders. Thus, the COVID-19 mechanisms for stimulating cognitive dysfunction may include neuroinflammation, which is mediated by a sustained systemic inflammation, a disrupted brain barrier, and severe glial reactiveness, especially within the limbic system. This review explores the interplay of infected lungs and brain in COVID-19 and its impact on the cognitive function.
许多 2019 冠状病毒病（COVID-19）康复患者报告出现神经系统、精神和认知问题的迹象和症状。然而，认知后遗症的确切患病率和结果尚不清楚。尽管严重急性呼吸综合征冠状病毒 2 通过与血管紧张素转换酶 2（ACE2）受体结合在急性感染中靶向脑细胞，但多项研究表明，许多发生神经系统疾病的 COVID-19 患者的大脑中并未检测到该病毒。因此，刺激认知功能障碍的 COVID-19 机制可能包括神经炎症，这是由持续的全身炎症、大脑屏障破坏和严重的神经胶质反应介导的，特别是在边缘系统中。本综述探讨了 COVID-19 中受感染的肺部和大脑之间的相互作用及其对认知功能的影响。
