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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., Competing Interests: Declarations. Competing interests: The authors declare no competing interests., (© 2024. Springer-Verlag GmbH Germany, part of Springer Nature.)