Can sars-cov-2 infection exacerbate Alzheimer’s disease? A systematic review

Chiara, Villa; Angelopoulou, Efthalia; Piperi, Christina

Background and aims: The ongoing coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus (SARS-CoV)-2 is having unprecedented effects in healthcare systems, economies and society. Although the respiratory tract is the primary target of SARS-CoV-2, emerging evidence suggests that the virus may also invade the central nervous system (CNS), leading to numerous neurological issues. In particular, people with Alzheimer's disease (AD) are vulnerable group at risk of contracting COVID-19 and present more severe forms and worse outcomes. Given the high prevalence of AD individuals affected by COVID-19, the aim of was to review common underlying etiological factors that may contribute to the acceleration of neurodegenerative processes in SARS-CoV-2-infected patients. Methods: PubMed database was searched for publications before 1st April 2021 using the keywords: “Alzheimer's disease” AND “COVID-19” AND “SARS-CoV-2”. Results: Inflammatory biomarkers, including IL-1, IL-6 and galectin-3 (Gal-3) are associated with high risk for developing COVID-19 and with the progression of AD. Moreover, SARS-CoV-2 infection exhibit high plasma levels of neurofilament light chain protein (NfL) and glial fibrillary acidic protein (GFAP), known as biochemical indicators of neuronal injury and glial activation in AD. Interestingly, the presence of the Apolipoprotein E (APOE) ε4 allele represents a risk factor for both diseases. Conclusions: Current literature suggests the existence of a synergistic relationship between COVID-19 and AD. The identification of potential biomarkers for the early identification of COVID-19 in patients with high risk of developing AD as well as the management and development of novel therapeutic strategies against both diseases.