tetano
Editor, Senior Moderator
Neuroimmunomodulation
. 2022 Nov 2;1-13.
doi: 10.1159/000526653. Online ahead of print.
The Infected Lungs and Brain Interface in COVID-19: The Impact on Cognitive Function
Larissa Joaquim[SUP] 1 [/SUP], Amanda Della Giustina[SUP] 2 [/SUP], Richard Simon Machado[SUP] 1 [/SUP], Kiuanne Lino Lobo Metzker[SUP] 1 [/SUP], Sandra Bonfante[SUP] 1 [/SUP], Lucineia Gainski Danielski[SUP] 3 [/SUP], Mariana Pereira de Souza Goldim[SUP] 1 [/SUP], Fabricia Petronilho[SUP] 3 [/SUP]
Affiliations
Abstract
Many coronavirus disease 2019 (COVID-19)-recovered patients report signs and symptoms and are experiencing neurological, psychiatric, and cognitive problems. However, the exact prevalence and outcome of cognitive sequelae is unclear. Even though the severe acute respiratory syndrome coronavirus 2 has target brain cells through binding to angiotensin-converting enzyme 2 (ACE2) receptor in acute infection, several studies indicate the absence of the virus in the brain of many COVID-19 patients who developed neurological disorders. Thus, the COVID-19 mechanisms for stimulating cognitive dysfunction may include neuroinflammation, which is mediated by a sustained systemic inflammation, a disrupted brain barrier, and severe glial reactiveness, especially within the limbic system. This review explores the interplay of infected lungs and brain in COVID-19 and its impact on the cognitive function.
Keywords: COVID-19; Cognitive dysfunction; Neuroinflammation; SARS-CoV-2.
. 2022 Nov 2;1-13.
doi: 10.1159/000526653. Online ahead of print.
The Infected Lungs and Brain Interface in COVID-19: The Impact on Cognitive Function
Larissa Joaquim[SUP] 1 [/SUP], Amanda Della Giustina[SUP] 2 [/SUP], Richard Simon Machado[SUP] 1 [/SUP], Kiuanne Lino Lobo Metzker[SUP] 1 [/SUP], Sandra Bonfante[SUP] 1 [/SUP], Lucineia Gainski Danielski[SUP] 3 [/SUP], Mariana Pereira de Souza Goldim[SUP] 1 [/SUP], Fabricia Petronilho[SUP] 3 [/SUP]
Affiliations
- PMID: 36323239
- DOI: 10.1159/000526653
Abstract
Many coronavirus disease 2019 (COVID-19)-recovered patients report signs and symptoms and are experiencing neurological, psychiatric, and cognitive problems. However, the exact prevalence and outcome of cognitive sequelae is unclear. Even though the severe acute respiratory syndrome coronavirus 2 has target brain cells through binding to angiotensin-converting enzyme 2 (ACE2) receptor in acute infection, several studies indicate the absence of the virus in the brain of many COVID-19 patients who developed neurological disorders. Thus, the COVID-19 mechanisms for stimulating cognitive dysfunction may include neuroinflammation, which is mediated by a sustained systemic inflammation, a disrupted brain barrier, and severe glial reactiveness, especially within the limbic system. This review explores the interplay of infected lungs and brain in COVID-19 and its impact on the cognitive function.
Keywords: COVID-19; Cognitive dysfunction; Neuroinflammation; SARS-CoV-2.