Potential hypothesis for the increased risk of Parkinson´s disease following COVID-19.

Patients with severe COVID-19 may be more likely to develop PD as a result of shared biological pathways including a great expansion of MDSCs and an imbalance in Th17/Tregs ratio. We think that these shared pathogenic features may mechanistically explain the COVID-19 - PD axis. Thus, we assume that patients who recovered from critical COVID-19 should be selected based upon a potential higher risk of developing PD. Further studies are needed to better define the possible relationship between COVID-19 and neuroinflammation and identify whether some people are more likely to develop PD after contracting COVID-19 than others with special emphasis to ascertain possible vulnerable genetic backgrounds or epigenetic factors acting on brain which may promote PD during SARS COV-2 infection. Finally, we think that regular physical activity should be performed and encouraged in patients with PD.

Alzheimer's disease following COVID-19: a two player match?

Common pathways may underlie the association between COVID-19 and risk for Alzheimer's disease (AD). We conjecture that severe COVID-19 may contribute to AD onset in predisposed individuals through aberrant MDSCs expression and increased IL-6 expression levels leading to immunosuppression in inflamed brains. Research studies are needed to gain empirical evidence to strengthen the hypothesis of the involvement of MDSCs and IL-6 in the formation of AD following COVID-19 infection and possibly vaccination enabling a more in-depth understanding of the role of immunosuppression in the onset of neurodegenerative diseases at any age. Identifying why those who get severe COVID-19 are more likely to develop AD may offer a novel therapeutic approach to delay or prevent cognitive decline.

Myocarditis and pericarditis following mRNA COVID-19 vaccination in younger patients: is there a shared thread?

Rare cases of myocarditis and pericarditis after COVID-19 mRNA vaccination have been recently reported in male adolescents and young adults. Acute myocarditis and pericarditis following COVID-19 mRNA vaccination in male adolescents and young adults may be connected with age-related lower levels of T-bet and PD-1 in predisposed individulas with T-bet polymorphisms by the release od autoreactive CD8+CTL. Upregulatiomn of T-Bet and PD-1 by estrogen might explai the higher incidence of men developing myocarditis or pericarditis in comparison to women.