tetano
Editor, Senior Moderator
J Neuroinflammation
. 2020 Sep 30;17(1):286.
doi: 10.1186/s12974-020-01957-4.
Neurological consequences of COVID-19: what have we learned and where do we go from here?
Abbas Jarrahi[SUP] 1 [/SUP], Meenakshi Ahluwalia[SUP] 2 [/SUP], Hesam Khodadadi[SUP] 3 [/SUP], Evila da Silva Lopes Salles[SUP] 3 [/SUP], Ravindra Kolhe[SUP] 2 [/SUP], David C Hess[SUP] 4 [/SUP], Fernando Vale[SUP] 1 [/SUP], Manish Kumar[SUP] 5 [/SUP], Babak Baban[SUP] 3 [/SUP], Kumar Vaibhav[SUP] 1 [/SUP], Krishnan M Dhandapani[SUP] 6 [/SUP]
Affiliations
Abstract
The coronavirus disease-19 (COVID-19) pandemic is an unprecedented worldwide health crisis. COVID-19 is caused by SARS-CoV-2, a highly infectious pathogen that is genetically similar to SARS-CoV. Similar to other recent coronavirus outbreaks, including SARS and MERS, SARS-CoV-2 infected patients typically present with fever, dry cough, fatigue, and lower respiratory system dysfunction, including high rates of pneumonia and acute respiratory distress syndrome (ARDS); however, a rapidly accumulating set of clinical studies revealed atypical symptoms of COVID-19 that involve neurological signs, including headaches, anosmia, nausea, dysgeusia, damage to respiratory centers, and cerebral infarction. These unexpected findings may provide important clues regarding the pathological sequela of SARS-CoV-2 infection. Moreover, no efficacious therapies or vaccines are currently available, complicating the clinical management of COVID-19 patients and emphasizing the public health need for controlled, hypothesis-driven experimental studies to provide a framework for therapeutic development. In this mini-review, we summarize the current body of literature regarding the central nervous system (CNS) effects of SARS-CoV-2 and discuss several potential targets for therapeutic development to reduce neurological consequences in COVID-19 patients.
Keywords: ARDS; Coagulopathy; Coronavirus; Cytokine storm; Neuroinflammation; Neurotropism; Neutrophil extracellular traps; SARS-CoV-2; Stroke.
. 2020 Sep 30;17(1):286.
doi: 10.1186/s12974-020-01957-4.
Neurological consequences of COVID-19: what have we learned and where do we go from here?
Abbas Jarrahi[SUP] 1 [/SUP], Meenakshi Ahluwalia[SUP] 2 [/SUP], Hesam Khodadadi[SUP] 3 [/SUP], Evila da Silva Lopes Salles[SUP] 3 [/SUP], Ravindra Kolhe[SUP] 2 [/SUP], David C Hess[SUP] 4 [/SUP], Fernando Vale[SUP] 1 [/SUP], Manish Kumar[SUP] 5 [/SUP], Babak Baban[SUP] 3 [/SUP], Kumar Vaibhav[SUP] 1 [/SUP], Krishnan M Dhandapani[SUP] 6 [/SUP]
Affiliations
- PMID: 32998763
- DOI: 10.1186/s12974-020-01957-4
Abstract
The coronavirus disease-19 (COVID-19) pandemic is an unprecedented worldwide health crisis. COVID-19 is caused by SARS-CoV-2, a highly infectious pathogen that is genetically similar to SARS-CoV. Similar to other recent coronavirus outbreaks, including SARS and MERS, SARS-CoV-2 infected patients typically present with fever, dry cough, fatigue, and lower respiratory system dysfunction, including high rates of pneumonia and acute respiratory distress syndrome (ARDS); however, a rapidly accumulating set of clinical studies revealed atypical symptoms of COVID-19 that involve neurological signs, including headaches, anosmia, nausea, dysgeusia, damage to respiratory centers, and cerebral infarction. These unexpected findings may provide important clues regarding the pathological sequela of SARS-CoV-2 infection. Moreover, no efficacious therapies or vaccines are currently available, complicating the clinical management of COVID-19 patients and emphasizing the public health need for controlled, hypothesis-driven experimental studies to provide a framework for therapeutic development. In this mini-review, we summarize the current body of literature regarding the central nervous system (CNS) effects of SARS-CoV-2 and discuss several potential targets for therapeutic development to reduce neurological consequences in COVID-19 patients.
Keywords: ARDS; Coagulopathy; Coronavirus; Cytokine storm; Neuroinflammation; Neurotropism; Neutrophil extracellular traps; SARS-CoV-2; Stroke.