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
影响因子:
4.7
通讯作者:
Ferreira ST
中科院分区:
文献类型:
--
作者:
Lyra E Silva NM;Barros-Aragão FGQ;De Felice FG;Ferreira ST
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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影响因子:
13.6
作者:
通讯作者:
--
影响因子:
4.4
作者:
Alenina, Natalia;Bader, Michael
通讯作者:
Bader, Michael
DOI:
10.1002/path.5056
发表时间:
2018-05
期刊:
The Journal of pathology
影响因子:
--
作者:
Batista AF;Forny-Germano L;Clarke JR;Lyra E Silva NM;Brito-Moreira J;Boehnke SE;Winterborn A;Coe BC;Lablans A;Vital JF;Marques SA;Martinez AM;Gralle M;Holscher C;Klein WL;Houzel JC;Ferreira ST;Munoz DP;De Felice FG
通讯作者:
De Felice FG
影响因子:
15.1
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Burton, Michael D.;Johnson, Rodney W.
通讯作者:
Johnson, Rodney W.
影响因子:
6.1
作者:
Basak JM;Ferreiro A;Cohen LS;Sheehan PW;Nadarajah CJ;Kanan MF;Sukhum KV;Dantas G;Musiek ES
通讯作者:
Musiek ES