Inflammation at the crossroads of COVID-19, cognitive deficits and depression.

Inflammation at the crossroads of COVID-19, cognitive deficits and depression.
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DOI:
10.1016/j.neuropharm.2022.109023
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发表时间:
2022-05-15
期刊:
影响因子:
4.7
通讯作者:
Ferreira ST
Ferreira ST
中科院分区:
医学2区
文献类型:
--
作者:
Lyra E Silva NM;Barros-Aragão FGQ;De Felice FG;Ferreira ST

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急性神经系统改变与 SARS-CoV-2 感染有关。此外,越来越明显的是,2019 年冠状病毒病 (COVID-19) 幸存者可能会出现长期的神经系统异常,包括认知缺陷和情绪改变。目前正在积极研究 COVID-19 对大脑造成急性和长期影响的机制。由于神经系统结果的异质性表现,SARS-CoV-2 感染后可能有不同的机制发挥作用,其中可能包括 SARS-CoV-2 的直接脑部感染、过度炎症性全身性疾病引起的机制或两者的组合。炎症是 COVID-19 的核心特征,已知中枢和全身炎症都会导致其他疾病的急性和持续性神经系统改变。在这里,我们回顾了表明 COVID-19 与神经炎症以及血脑屏障功能障碍有关的证据。类似的神经炎症特征与阿尔茨海默病和重度抑郁症有关。目前的证据表明,已有认知和神经精神缺陷的患者在感染 SARS-CoV-2 后表现出更差的结果,相反,COVID-19 幸存者患痴呆和情绪障碍的风险可能增加。考虑到世界范围内从感染中恢复的 COVID-19 患者的高患病率以及对痴呆症和抑郁症患病率的惊人预测,对这些疾病之间可能的分子相似性的研究可能会揭示导致 COVID-19 幸存者长期神经系统异常的机制。本文是“外设与大脑的串扰”特刊的一部分。
Acute neurological alterations have been associated with SARS-CoV-2 infection. Additionally, it is becoming clear that coronavirus disease 2019 (COVID-19) survivors may experience long-term neurological abnormalities, including cognitive deficits and mood alterations. The mechanisms underlying acute and long-term impacts of COVID-19 in the brain are being actively investigated. Due to the heterogeneous manifestations of neurological outcomes, it is possible that different mechanisms operate following SARS-CoV-2 infection, which may include direct brain infection by SARS-CoV-2, mechanisms resulting from hyperinflammatory systemic disease, or a combination of both. Inflammation is a core feature of COVID-19, and both central and systemic inflammation are known to lead to acute and persistent neurological alterations in other diseases. Here, we review evidence indicating that COVID-19 is associated with neuroinflammation, along with blood-brain barrier dysfunction. Similar neuroinflammatory signatures have been associated with Alzheimer's disease and major depressive disorder. Current evidence demonstrates that patients with pre-existing cognitive and neuropsychiatric deficits show worse outcomes upon infection by SARS-CoV-2 and, conversely, COVID-19 survivors may be at increased risk of developing dementia and mood disorders. Considering the high prevalence of COVID-19 patients that recovered from infection in the world and the alarming projections for the prevalence of dementia and depression, investigation of possible molecular similarities between those diseases may shed light on mechanisms leading to long-term neurological abnormalities in COVID-19 survivors. This article is part of the special Issue on ‘Cross Talk between Periphery and the Brain’.
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