tetano
Editor, Senior Moderator
Mol Neurobiol
. 2021 Jun 1.
doi: 10.1007/s12035-021-02438-2. Online ahead of print.
The Effect of COVID-19 on NF-κB and Neurological Manifestations of Disease
Don A Davies[SUP] 1 [/SUP], Aida Adlimoghaddam[SUP] 2 [/SUP], Benedict C Albensi[SUP] 3 4 [/SUP]
Affiliations
Abstract
The coronavirus disease that presumably began in 2019 (COVID-19) is a highly infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has resulted in a pandemic. Initially, COVID-19 was thought to only affect respiration. However, accumulating evidence shows a wide range of neurological symptoms are also associated with COVID-19, such as anosmia/ageusia, headaches, seizures, demyelination, mental confusion, delirium, and coma. Neurological symptoms in COVID-19 patients may arise due to a cytokine storm and a heighten state of inflammation. The nuclear factor kappa-light-chain enhancer of activated B cells (NF-κB) is a central pathway involved with inflammation and is shown to be elevated in a dose-dependent matter in response to coronaviruses. NF-κB has a role in cytokine storm syndrome, which is associated with greater severity in COVID-19-related symptoms. Therefore, therapeutics that reduce the NF-κB pathway should be considered in the treatment of COVID-19. Neuro-COVID-19 units have been established across the world to examine the neurological symptoms associated with COVID-19. Neuro-COVID-19 is increasingly becoming an accepted term among scientists and clinicians, and interdisciplinary teams should be created to implement strategies for treating the wide range of neurological symptoms observed in COVID-19 patients.
Keywords: COVID-19; Cognitive impairment; NF-κB; Neuro-COVID-19; Oxidative stress.
. 2021 Jun 1.
doi: 10.1007/s12035-021-02438-2. Online ahead of print.
The Effect of COVID-19 on NF-κB and Neurological Manifestations of Disease
Don A Davies[SUP] 1 [/SUP], Aida Adlimoghaddam[SUP] 2 [/SUP], Benedict C Albensi[SUP] 3 4 [/SUP]
Affiliations
- PMID: 34075562
- DOI: 10.1007/s12035-021-02438-2
Abstract
The coronavirus disease that presumably began in 2019 (COVID-19) is a highly infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has resulted in a pandemic. Initially, COVID-19 was thought to only affect respiration. However, accumulating evidence shows a wide range of neurological symptoms are also associated with COVID-19, such as anosmia/ageusia, headaches, seizures, demyelination, mental confusion, delirium, and coma. Neurological symptoms in COVID-19 patients may arise due to a cytokine storm and a heighten state of inflammation. The nuclear factor kappa-light-chain enhancer of activated B cells (NF-κB) is a central pathway involved with inflammation and is shown to be elevated in a dose-dependent matter in response to coronaviruses. NF-κB has a role in cytokine storm syndrome, which is associated with greater severity in COVID-19-related symptoms. Therefore, therapeutics that reduce the NF-κB pathway should be considered in the treatment of COVID-19. Neuro-COVID-19 units have been established across the world to examine the neurological symptoms associated with COVID-19. Neuro-COVID-19 is increasingly becoming an accepted term among scientists and clinicians, and interdisciplinary teams should be created to implement strategies for treating the wide range of neurological symptoms observed in COVID-19 patients.
Keywords: COVID-19; Cognitive impairment; NF-κB; Neuro-COVID-19; Oxidative stress.