Dissecting the Molecular Mechanisms Surrounding Post-COVID-19 Syndrome and Neurological Features, Mohamed et al, 2022

International Journal of Molecular Sciences
Dissecting the Molecular Mechanisms Surrounding Post-COVID-19 Syndrome and Neurological Features - Mohamed et al

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.

Furthermore, 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 hypothalamic 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.

 

Spotted this on Twitter via prof. Kunst who comments:

A new review suggests that #LongCovid may be "partially explained by a neuroinflammatory process involving the activation of astrocytes and microglia."

Haven't read the study myself, but see there are some mentions about ME as well.