PDF(Pubmed)
Abstract：
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.
摘要：
与2019年冠状病毒病(COVID-19)相关的认知能力下降的可能性和严重程度已被证明反映在感染的严重程度和特定生物标志物的伴随变化上。本综述讨论了microRNAs（miRNAs/miRs）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。从2000年1月31日至2022年12月31日，使用PubMed对已发表的文章进行了系统的搜索，ProQuest,科学直接和谷歌学者数据库，结合以下术语：\'COVID-19\'或\'SARS-CoV-2\'或\'COVID-19后效应\'或\'认知下降\'或\'神经变性\'或\'microRNAs\'。证据质量评价高,中度,低,或基于等级评级非常低。总共确定了36项研究，这些研究表明miR-146a的血液水平降低。miR-155，Let-7b，与健康组相比，COVID-19患者的miR-31和miR-21。Let-7b的过度表达可能通过调节慢性炎症性疾病之间的免疫反应，导致COVID-9期间BCL-2的下调，2型糖尿病,COVID-19与认知障碍。miR-31的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能力增加有关。miR-155介导突触功能障碍和急性炎症引起的神经递质失调，导致脑萎缩和皮质下认知特征.miR-21在COVID-19患者中的下调会加重全身炎症反应，介导无法控制的免疫反应和T细胞功能的失败，引起SARS-CoV-2患者的认知障碍。总的来说,本综述表明miR-146a水平失调，miR-155，Let-7b，COVID-19患者血液中的miR-31和miR-21与认知能力下降有关，免疫机制的慢性激活，细胞因子风暴，以及损害和全身炎症的恶性循环。
