Bougea Anastasia, Georgakopoulou Vasiliki Epameinondas, Lempesis Ioannis G, Fotakopoulos George, Papalexis Petros, Sklapani Pagona, Trakas Nikolaos, Spandidos Demetrios A, Angelopoulou Efthalia
1st Department of Neurology, Eginition Hospital, School of Medicine, National and Kapodistrian University of Athens, 11528 Athens, Greece.
Department of Pathophysiology, Laiko General Hospital, National and Kapodistrian University of Athens, 11527 Athens, Greece.
Exp Ther Med. 2024 Feb 14;27(4):139. doi: 10.3892/etm.2024.12427. eCollection 2024 Apr.
The likelihood and severity of cognitive decline related to coronavirus disease 2019 (COVID-19) have been shown to be reflected by the severity of the infection and concomitant alterations in specific biomarkers. The present review discusses the role of microRNAs (miRNAs/miRs) as biomarkers in COVID-19 and the potential molecular mechanisms of cognitive dysfunction related to COVID-19. A systematic search of published articles was carried out from January 31, 2000 to December 31, 2022 using the PubMed, ProQuest, Science Direct and Google Scholar databases, combining the following terms: 'COVID-19' OR 'SARS-CoV-2' OR 'post-COVID-19 effects' OR 'cognitive decline' OR 'neurodegeneration' OR 'microRNAs'. The quality of the evidence was evaluated as high, moderate, low, or very low based on the GRADE rating. A total of 36 studies were identified which demonstrated reduced blood levels of miR-146a, miR-155, Let-7b, miR 31 and miR-21 in patients with COVID-19 in comparison with a healthy group. The overexpression of the Let-7b may result in the downregulation of BCL-2 during COVID-9 by adjusting the immune responses between chronic inflammatory disease, type 2 diabetes, COVID-19 and cognitive impairment. The reduced expression of miR-31 is associated with cognitive dysfunction and increased microcoagulability in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). miR-155 mediates synaptic dysfunction and the dysregulation of neurotransmitters due to acute inflammation, leading to brain atrophy and a subcortical cognitive profile. The downregulation of miR-21 in patients with COVID-19 aggravates systemic inflammation, mediating an uncontrollable immune response and the failure of T-cell function, provoking cognitive impairment in patients with SARS-CoV-2. On the whole, the present review indicates that dysregulated levels of miR-146a, miR-155, Let-7b, miR-31, and miR-21 in the blood of individuals with COVID-19 are associated with cognitive decline, the chronic activation of immune mechanisms, the cytokine storm, and the vicious cycle of damage and systemic inflammation.
2019年冠状病毒病（COVID-19）相关认知功能下降的可能性和严重程度已被证明可通过感染的严重程度以及特定生物标志物的伴随变化来反映。本综述讨论了微小RNA（miRNA/miR）作为COVID-19生物标志物的作用以及与COVID-19相关的认知功能障碍的潜在分子机制。使用PubMed、ProQuest、Science Direct和谷歌学术数据库，对2000年1月31日至2022年12月31日发表的文章进行了系统检索，组合了以下关键词：“COVID-19”或“SARS-CoV-2”或“COVID-19后效应”或“认知功能下降”或“神经退行性变”或“微小RNA”。根据GRADE评级，将证据质量评估为高、中、低或极低。共确定了36项研究，这些研究表明，与健康组相比，COVID-19患者血液中miR-146a、miR-155、Let-7b、miR-31和miR-21的水平降低。Let-7b的过表达可能通过调节慢性炎症性疾病、2型糖尿病、COVID-19和认知障碍之间的免疫反应，导致COVID-19期间BCL-2的下调。miR-31表达降低与严重急性呼吸综合征冠状病毒2（SARS-CoV-2）患者的认知功能障碍和微凝血增加有关。miR-155介导急性炎症引起的突触功能障碍和神经递质失调，导致脑萎缩和皮质下认知特征。COVID-19患者中miR-21的下调会加剧全身炎症，介导无法控制的免疫反应和T细胞功能衰竭，引发SARS-CoV-2患者的认知障碍。总体而言，本综述表明，COVID-19患者血液中miR-
