LSU Neuroscience Center, Louisiana State University Health Science Center, New Orleans, LA 70112, USA.
Alchem Biotek Research, Toronto, ON M5S 1A8, Canada.
Biomolecules. 2022 Sep 7;12(9):1253. doi: 10.3390/biom12091253.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of the COVID-19 disease, is a highly infectious and transmissible viral pathogen that continues to impact human health globally. Nearly ~600 million people have been infected with SARS-CoV-2, and about half exhibit some degree of continuing health complication, generically referred to as long COVID. Lingering and often serious neurological problems for patients in the post-COVID-19 recovery period include brain fog, behavioral changes, confusion, delirium, deficits in intellect, cognition and memory issues, loss of balance and coordination, problems with vision, visual processing and hallucinations, encephalopathy, encephalitis, neurovascular or cerebrovascular insufficiency, and/or impaired consciousness. Depending upon the patient’s age at the onset of COVID-19 and other factors, up to ~35% of all elderly COVID-19 patients develop a mild-to-severe encephalopathy due to complications arising from a SARS-CoV-2-induced cytokine storm and a surge in cytokine-mediated pro-inflammatory and immune signaling. In fact, this cytokine storm syndrome: (i) appears to predispose aged COVID-19 patients to the development of other neurological complications, especially those who have experienced a more serious grade of COVID-19 infection; (ii) lies along highly interactive and pathological pathways involving SARS-CoV-2 infection that promotes the parallel development and/or intensification of progressive and often lethal neurological conditions, and (iii) is strongly associated with the symptomology, onset, and development of human prion disease (PrD) and other insidious and incurable neurological syndromes. This commentary paper will evaluate some recent peer-reviewed studies in this intriguing area of human SARS-CoV-2-associated neuropathology and will assess how chronic, viral-mediated changes to the brain and CNS contribute to cognitive decline in PrD and other progressive, age-related neurodegenerative disorders.
严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）是导致 COVID-19 疾病的病原体，是一种高度传染性和可传播的病毒病原体，继续对全球人类健康造成影响。近 6 亿人感染了 SARS-CoV-2，约有一半人出现某种程度的持续健康并发症，通常称为长 COVID。在 COVID-19 恢复期的患者中，挥之不去且经常出现严重的神经问题包括脑雾、行为变化、意识模糊、谵妄、智力缺陷、认知和记忆问题、失去平衡和协调能力、视力问题、视觉处理和幻觉、脑病、脑炎、神经血管或脑血管功能不全以及/或意识障碍。根据 COVID-19 发病时患者的年龄和其他因素，多达 35%的所有老年 COVID-19 患者会因 SARS-CoV-2 诱导的细胞因子风暴和细胞因子介导的促炎和免疫信号的激增而导致 COVID-19 引起的轻度至重度脑病。实际上，这种细胞因子风暴综合征：（i）似乎使老年 COVID-19 患者易患其他神经并发症，尤其是那些经历过更严重 COVID-19 感染的患者；（ii）沿着高度相互作用和病理途径发生，涉及 SARS-CoV-2 感染，可促进进行性和经常致命的神经疾病的平行发展和/或加剧；（iii）与人类朊病毒病（PrD）和其他隐匿和无法治愈的神经综合征的症状、发作和发展密切相关。本评论文章将评估人类 SARS-CoV-2 相关神经病理学这一有趣领域的一些最近同行评审研究，并评估慢性、病毒介导的大脑和中枢神经系统变化如何导致 PrD 和其他进行性、与年龄相关的神经退行性疾病的认知能力下降。
