Treating neuroinflammation caused by Covd-19 to prevent neurodegenerative diseases. It is the approach to follow according to Arianna Di Stadio, neuroscientist Professor at the University of Catania and honorary researcher at the Neuroinflammation Laboratory of UCL Queen Square Neurology in London, also on the basis of a recent study published in the journal Nature.
The study identified a relationship between Covid-19 infection and neurodegenerative diseases and demonstrated how the treatment of neuroinflammation is able to inhibit this neurodegeneration. Researchers who developed a complex study using both the animal model and human microglia, a type of cell involved in active immune defense in the nervous system, found that SARS-CoV2 activates microglia in its inflammatory form and that this phenomenon persists even when the virus has been eradicated. However, the researchers discovered that using anti-neuroinflammatory drugs it was possible to block this process by increasing the survival of Sars-CoV2-infected mice that died from the neurological consequences of the virus, comparing them with untreated ones. The SarsCoV2 virus can then activate microglia causing the symptoms common to neurodegenerative diseases such as Parkinson’s.
The researchers tested molecules capable of limiting the activation of microglia after it was activated by Covid-19 and observed a reduction in symptoms. Since microglia, in its pro-inflammatory form, is responsible for several neurodegenerative and neuro-inflammatory diseases and can be deactivated in the experiment conducted, the researchers hypothesized that the treatment of neuro-inflammation could be a potential way of intervention also for Parkinson’s. This study “demonstrates at the cellular level what we have highlighted with our clinical studies, i.e. that using an anti-neuroinflammation molecule it is possible to modulate these cells which help the recovery of post-Covid olfactory and cognitive functions – says Di Stadio -. The study demonstrates how the virus is able to cause inflammation in the brain, even after the infection has resolved.
In simple words, although Covid creates neuro-inflammation, if this is resolved with treatment, both those who could be genetically more predisposed to developing a neurodegenerative disease will benefit, and those who, even if not genetically predisposed, could have a increased risk of developing it following SarsCoV2 infection. I believe that this discovery is absolutely a step forward not only to limit the possible long-term negative effects of the Covid infection but also an incentive to continue working on neuro-inflammation and its prevention as an ally to fight neuro-degenerative diseases” .
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