By
Source Frontiers
1. Introduction
The COVID-19 pandemic, caused by infection with the SARS-CoV-2 virus, is associated with patients suffering neurological symptoms including cognitive impairment (Hosp et al., 2021; Spudich and Nath, 2022; Taquet et al., 2022) plus an increase in the levels of dementia and Alzheimer’s disease (AD) progression (Chen et al., 2022; Gordon et al., 2022; Golzari-Sorkheh et al., 2023; Olivera et al., 2023). The SARS-CoV-2 genome and proteome have been sequenced and components of the virus targeted for diagnosis and therapy (Hu et al., 2021; Kukar et al., 2021; Mishra et al., 2021; Yadav et al., 2021). The SARS-CoV-2 spike protein forms a trimer (Wrapp et al., 2020) that binds the angiotensin-converting enzyme 2 (ACE2) receptor on host cell surfaces to gain entry into the cells (Benton et al., 2020). Mutations of the receptor binding domain of the SARS-CoV-2 spike protein are found in a number of the variants of concern that show altered binding to the ACE2 receptor (Kim et al., 2023) and this also influences neurological symptoms (Taquet et al., 2022). The SARS-CoV-2 virus has been found in post-mortem brains (Crunfli et al., 2022; Stein et al., 2022), but some studies have failed to detect it (Khan et al., 2022). The mechanism of SARS-CoV-2 entry into the brain may involve either transmission via the nasal cavity (Butowt and von Bartheld, 2022) and/or an impaired blood-brain barrier (Yang et al., 2022). The key question is if the SARS-CoV-2 virus itself causes dementia and/or if SARS-CoV-2 infection exacerbates existing dementia (Paterson et al., 2020; Danics et al., 2021; Ecarnot et al., 2023). Dementia has many forms (Garcia-Ptacek et al., 2014) and some forms are associated with infections (Shinjyo et al., 2021).
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