Dissecting the Molecular Mechanisms Surrounding Post‐COVID‐19 Syndrome and Neurological Features (Mohamed, 2022)

[Consul]

Abstract

Many of the survivors of the novel coronavirus disease (COVID‐19) are suffering from persistent symptoms, causing significant morbidity and decreasing their quality of life, termed “post‐COVID‐19 syndrome” or “long COVID”. Understanding the mechanisms surrounding PCS is vital to developing the diagnosis, biomarkers, and possible treatments. Here, we describe the prevalence and manifestations of PCS, and similarities with previous SARS epidemics. Further‐more, we look at the molecular mechanisms behind the neurological features of PCS, where we highlight important neural mechanisms that may potentially be involved and pharmacologically
targeted, such as glutamate reuptake in astrocytes, the role of NMDA receptors and transporters (EAAT2), ROS signaling, astrogliosis triggered by NF‐κB signaling, KNDy neurons, and hypotha-lamic networks involving Kiss1 (a ligand for the G‐protein coupled receptor 54 (GPR54)), among others. We highlight the possible role of reactive gliosis following SARS‐CoV‐2 CNS injury, as well as the potential role of the hypothalamus network in PCS manifestations.


The study (pdf file): https://mdpi-res.com/d_attachment/ijms/ijms-23-04275/article_deploy/ijms-23-04275.pdf

 

[Pyrrhus]

Thanks for posting this paper!

From the abstract:

We highlight the possible role of reactive gliosis following SARS‐CoV‐2 CNS injury

"reactive gliosis" is just a very old term for "neuroinflammation"


And from the body of the paper:

A long‐term follow‐up study after the SARS outbreak in 2003 found that 40% of respondents reported chronic fatigue and 27% met the criteria for chronic fatigue syndrome (ME/CFS) diagnosis, while mental disorders were reported by 40% of respondents [34].

P.S.
Full list of authors: Mohamed S. Mohamed, Anton Johansson, Jörgen Jonsson † and Helgi B. Schiöth *,†

 

[SWAlexander]

Thanks for posting this paper!

From the abstract:

"reactive gliosis" is just a very old term for "neuroinflammation"


And from the body of the paper:



P.S.
Full list of authors: Mohamed S. Mohamed, Anton Johansson, Jörgen Jonsson † and Helgi B. Schiöth *,†

I wonder if an undetected very early CNS injury (traumatic brain injury or spinal cord injury) could be the gateway (higher vulnerability) to neuroinflammation by infections.