Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.10.08.331157v1?rss=1 Authors: Suzuki, Y. J., Ding, Q., Shults, N. V., Harris, B. T. Abstract: Alzheimers disease is a chronic neurodegenerative disorder and represents the main cause of dementia. Currently, the world is suffering from the pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that uses angiotensin-converting enzyme 2 (ACE2) as a receptor to enter the host cells. In COVID-19, neurological manifestations have been reported to occur. The present study demonstrates that the protein expression level of ACE2 is upregulated in the brain of Alzheimers disease patients. The increased ACE2 expression is not age-dependent, suggesting the direct relationship between Alzheimers disease and the ACE2 expression. Oxidative stress has been implicated in the pathogenesis of Alzheimers disease, and Alzheimers disease brains examined in this study also exhibited higher carbonylated proteins as well as increased thiol oxidation state of peroxiredoxin 6 (Prx6). The positive correlation was found between the increased ACE2 protein expression and oxidative stress in Alzheimers disease brain. Thus, the present study reveals the relationships between Alzheimers disease and ACE2, the receptor for SARS-CoV-2. These results warrant monitoring Alzheimers disease patients with COVID-19 carefully for the possible higher viral load in the brain and long-term adverse neurological consequences. Copy rights belong to original authors. Visit the link for more info