Mormile Raffaella, Mormile Cristina, Picone Carmine
Division of Pediatrics and Neonatology, Moscati Hospital, Via A. Gramsci, Aversa, 81031, Italy.
Sapienza University of Rome, Rome, Italy.
Infection. 2024 Dec;52(6):2547-2549. doi: 10.1007/s15010-024-02368-w. Epub 2024 Aug 14.
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.
共同途径可能是新冠病毒疾病（COVID-19）与阿尔茨海默病（AD）风险之间关联的基础。我们推测，严重的COVID-19可能通过异常的髓系来源抑制细胞（MDSCs）表达和白细胞介素-6（IL-6）表达水平升高，导致炎症大脑中的免疫抑制，从而促使易感个体患上AD。需要开展研究以获取实证证据，加强关于MDSCs和IL-6参与COVID-19感染及可能的疫苗接种后AD形成的假说，从而更深入地了解免疫抑制在任何年龄神经退行性疾病发病中的作用。弄清楚为何感染严重COVID-19的人更易患AD，可能会为延缓或预防认知衰退提供一种新的治疗方法。
