tetano
Editor, Senior Moderator
Curr Opin Pharmacol
. 2021 Dec 31;63:102181.
doi: 10.1016/j.coph.2021.12.008. Online ahead of print.
Neuroinflammation in Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) infection: Pathogenesis and clinical manifestations
Graciela Cárdenas[SUP] 1 [/SUP], Gladis Fragoso[SUP] 2 [/SUP], Edda Sciutto[SUP] 2 [/SUP]
Affiliations
Abstract
Peripheral inflammation and neuroinflammation are host-mounted to eliminate injury, infection, or toxin to restore homeostasis. However, when inflammation persists, it may promote collateral tissue damage that ultimately culminates in pathological peripheral damage or neurodegeneration. Since the beginning of the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) pandemic, responsible of Coronavirus disease 2019 (COVID-19), accumulating evidence describes neurological manifestations and complications worldwide particularly in approximately one-third of patients with COVID-19 particularly in those affected with the severe forms of the disease. Different access routes to the central nervous system have been identified. One immediately used is the entrance by the olfactory and trigeminus nervous affecting olfactory and sensory nerve endings when individuals get the infection by the intranasal route. It can also reach the central nervous system through the choroid plexuses and periventricular areas that lack blood-brain barrier or by its disruption by the exacerbated peripheral inflammation. Until now, the long-term sequelae of SARS-CoV-2 infection is still under research and the post-COVID syndrome. This review focuses on the consequences of the neuroinflammatory response in patients with COVID-19 considering its potential relevance in the appearance of neurological sequelae including neurodegenerative disorders.
. 2021 Dec 31;63:102181.
doi: 10.1016/j.coph.2021.12.008. Online ahead of print.
Neuroinflammation in Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) infection: Pathogenesis and clinical manifestations
Graciela Cárdenas[SUP] 1 [/SUP], Gladis Fragoso[SUP] 2 [/SUP], Edda Sciutto[SUP] 2 [/SUP]
Affiliations
- PMID: 35074661
- DOI: 10.1016/j.coph.2021.12.008
Abstract
Peripheral inflammation and neuroinflammation are host-mounted to eliminate injury, infection, or toxin to restore homeostasis. However, when inflammation persists, it may promote collateral tissue damage that ultimately culminates in pathological peripheral damage or neurodegeneration. Since the beginning of the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) pandemic, responsible of Coronavirus disease 2019 (COVID-19), accumulating evidence describes neurological manifestations and complications worldwide particularly in approximately one-third of patients with COVID-19 particularly in those affected with the severe forms of the disease. Different access routes to the central nervous system have been identified. One immediately used is the entrance by the olfactory and trigeminus nervous affecting olfactory and sensory nerve endings when individuals get the infection by the intranasal route. It can also reach the central nervous system through the choroid plexuses and periventricular areas that lack blood-brain barrier or by its disruption by the exacerbated peripheral inflammation. Until now, the long-term sequelae of SARS-CoV-2 infection is still under research and the post-COVID syndrome. This review focuses on the consequences of the neuroinflammatory response in patients with COVID-19 considering its potential relevance in the appearance of neurological sequelae including neurodegenerative disorders.