ABSTRACT
This letter discusses whether SARS-CoV-2 causes tauopathy. Tauopathies are characterized by the deposition of insoluble aggregated tau in neurons and, occasionally, glial cells. Tauopathies are classified as either primary, in which tau is thought to be the driver of disease, or secondary, in which tau aggregation is downstream of another insult. SARS-CoV-2 might cross the blood- brain barrier and directly infect neurons or the surrounding vasculature, as shown in non-human primates. Once inside cells, SARS-CoV-2 can directly activate the NLRP3 inflammasome and induce tau mislocalisation4 in human cells in vitro. A second possible mechanism by which SARS-CoV-2 could affect the CNS is through inducing a widespread systemic inflammatory response. Accumulated exposures to pathogens that contribute to neuroinflammation might increase the risk of developing a tauopathy. Only 0.01-0.1% of measles infections lead to subacute sclerosing panencephalitis. If a COVID-19-induced tauopathy develops at a similar rate, there could be 10 000-100 000 cases for every 100 million people infected with SARS-CoV-2. However, the proportion of individuals infected with SARS-CoV-2 who have substantial neuroinflammation, and who are therefore potentially at a higher risk of developing secondary tauopathy, is unknown. It is also important to note that no direct causal link between COVID-19 and neurological or psychiatric sequelae has been found, and some complications-including anxiety disorders-might be due to the stress and trauma associated with social factors and treatment options. (PsycInfo Database Record (c) 2021 APA, all rights reserved)