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.
View Article and Find Full Text PDFDirect oral anticoagulants (DOACs) are widely used for treatment and secondary prophylaxis of venous thromboembolism (VTE) and represent the gold standard for VTE secondary prophylaxis, with low-intensity DOACs administration becoming increasingly used worldwide in such scenario. Albeit widespread DOACs usage there are few literature data regarding their efficacy and safety in major thrombophilia carriers and almost no data is available for low intensity apixaban and rivaroxaban as secondary VTE prophylaxis in such patients. The aim of our study is to evaluate and confront the efficacy and safety of low-dose DOACs for VTE secondary prophylaxis, in major thrombophilia carriers vs patients at high risk of VTE recurrence for other reasons.
View Article and Find Full Text PDFCommon 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.
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