Following this hypothesis, researchers are now questioning whether coronavirus affects the brain, could pose a risk for neurodegenerative disorders further down the line, like Alzheimer’s or Parkinson’s.
Oher research demonstrated the mechanism of why the virus was able to gain access into the brain through the nose, but this was the first to demonstrate how the coronavirus activated the brain’s immune response.
The COVID-19 virus may not be multiplying in the brain, but when it gets into the brain, it can induce immune responses and this explains some of the trends people have reported when they have been infected such as continued brain fog and memory loss.
In this study, they investigated the effects of the SARS‐CoV‐2 spike protein S1 stimulation on neuroinflammation in brain nerve cells.
Results of the experiment show that the recombinant SARS-CoV-2 spike protein sub-unit S1 activated BV-2 microglia as demonstrated by an increase in the protein expression of Iba-1, which is mainly expressed by the microglia and increased by the activation of these cells.
Activation of neuroinflammatory processes by the spike S1 protein was further confirmed by results showing increased iNOS-mediated production of NO by the protein in brain cells.
Elevated iNOS/NO has been previously linked to a wide range of CNS disorders including Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, epilepsy, and migraine.
Further studies are therefore needed to elucidate the link between COVID-19-mediated hyper-inflammation and the pathogenesis of neurological symptoms that have been reported to be associated with the disease.
These results contribute to our understanding of some of the mechanisms involved in CNS pathologies of SARS-CoV-2.
Source: Medindia
