Owens Cameron D, Bonin Pinto Camila, Detwiler Sam, Olay Lauren, Pinaffi-Langley Ana Clara da C, Mukli Peter, Peterfi Anna, Szarvas Zsofia, James Judith A, Galvan Veronica, Tarantini Stefano, Csiszar Anna, Ungvari Zoltan, Kirkpatrick Angelia C, Prodan Calin I, Yabluchanskiy Andriy
Oklahoma Center for Geroscience and Healthy Brain Aging, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73117, USA.
Vascular Cognitive Impairment, Neurodegeneration and Healthy Brain Aging Program, Department of Neurosurgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.
Brain Commun. 2024 Mar 7;6(2):fcae080. doi: 10.1093/braincomms/fcae080. eCollection 2024.
Components that comprise our brain parenchymal and cerebrovascular structures provide a homeostatic environment for proper neuronal function to ensure normal cognition. Cerebral insults (e.g. ischaemia, microbleeds and infection) alter cellular structures and physiologic processes within the neurovascular unit and contribute to cognitive dysfunction. COVID-19 has posed significant complications during acute and convalescent stages in multiple organ systems, including the brain. Cognitive impairment is a prevalent complication in COVID-19 patients, irrespective of severity of acute SARS-CoV-2 infection. Moreover, overwhelming evidence from in vitro, preclinical and clinical studies has reported SARS-CoV-2-induced pathologies in components of the neurovascular unit that are associated with cognitive impairment. Neurovascular unit disruption alters the neurovascular coupling response, a critical mechanism that regulates cerebromicrovascular blood flow to meet the energetic demands of locally active neurons. Normal cognitive processing is achieved through the neurovascular coupling response and involves the coordinated action of brain parenchymal cells (i.e. neurons and glia) and cerebrovascular cell types (i.e. endothelia, smooth muscle cells and pericytes). However, current work on COVID-19-induced cognitive impairment has yet to investigate disruption of neurovascular coupling as a causal factor. Hence, in this review, we aim to describe SARS-CoV-2's effects on the neurovascular unit and how they can impact neurovascular coupling and contribute to cognitive decline in acute and convalescent stages of the disease. Additionally, we explore potential therapeutic interventions to mitigate COVID-19-induced cognitive impairment. Given the great impact of cognitive impairment associated with COVID-19 on both individuals and public health, the necessity for a coordinated effort from fundamental scientific research to clinical application becomes imperative. This integrated endeavour is crucial for mitigating the cognitive deficits induced by COVID-19 and its subsequent burden in this especially vulnerable population.
构成我们脑实质和脑血管结构的成分，为神经元正常功能提供了一个稳态环境，以确保正常认知。脑部损伤（如缺血、微出血和感染）会改变神经血管单元内的细胞结构和生理过程，并导致认知功能障碍。新冠病毒病在包括大脑在内的多个器官系统的急性期和恢复期都引发了严重并发症。认知障碍是新冠病毒病患者中普遍存在的并发症，与急性严重急性呼吸综合征冠状病毒2感染的严重程度无关。此外，来自体外、临床前和临床研究的大量证据表明，严重急性呼吸综合征冠状病毒2会在神经血管单元的组成部分中引发与认知障碍相关的病变。神经血管单元破坏会改变神经血管耦合反应，这是一种调节脑微血管血流以满足局部活跃神经元能量需求的关键机制。正常的认知过程是通过神经血管耦合反应实现的，涉及脑实质细胞（即神经元和神经胶质细胞）和脑血管细胞类型（即内皮细胞、平滑肌细胞和周细胞）的协同作用。然而，目前关于新冠病毒病所致认知障碍的研究尚未将神经血管耦合破坏作为一个因果因素进行调查。因此，在本综述中，我们旨在描述严重急性呼吸综合征冠状病毒2对神经血管单元的影响，以及它们如何在疾病的急性期和恢复期影响神经血管耦合并导致认知衰退。此外，我们还探讨了减轻新冠病毒病所致认知障碍的潜在治疗干预措施。鉴于与新冠病毒病相关的认知障碍对个人和公共卫生都有巨大影响，从基础科学研究到临床应用进行协同努力变得势在必行。这种综合努力对于减轻新冠病毒病所致的认知缺陷及其在这一特别脆弱人群中的后续负担至关重要。
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