Abstract
The current coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus (SARS-CoV)-2, is affecting every aspect of global society, including public healthcare systems, medical care access, and the economy. Although the respiratory tract is primarily affected by SARS-CoV-2, emerging evidence suggests that the virus may also reach the central nervous system (CNS), leading to several neurological issues. In particular, people with a diagnosis of Alzheimer’s disease (AD) are a vulnerable group at high risk of contracting COVID-19, and develop more severe forms and worse outcomes, including death. Therefore, understanding shared links between COVID-19 and AD could aid the development of therapeutic strategies against both. Herein, we reviewed common risk factors and potential pathogenetic mechanisms that might contribute to the acceleration of neurodegenerative processes in AD patients infected by SARS-CoV-2.
Highlights
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), continues to spread rapidly across the globe, becoming a devastating pandemic infection with growing mortality rates [1]
Both human and animal models demonstrated that the virus can directly invade the olfactory bulb [11] without a primary lung involvement, by the interaction between the virus S1 spike protein and angiotensin-converting enzyme 2 (ACE2), which is widely expressed in the glial cells and neurons [12]
Epidemiological data from China showed that the case fatality ratio (CFR) of COVID-19 increases with age [24]; patients aged 59 years or older were at least 5 times more prone to die after the development of symptoms than younger ones [25]
Summary
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), continues to spread rapidly across the globe, becoming a devastating pandemic infection with growing mortality rates [1]. A neurochemical study reported that patients with severe SARS-CoV-2 infections 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 [10], further supporting a direct link between SARS-CoV-2 brain infection and neurological disturbances Both human and animal models demonstrated that the virus can directly invade the olfactory bulb [11] without a primary lung involvement, by the interaction between the virus S1 spike protein and angiotensin-converting enzyme 2 (ACE2), which is widely expressed in the glial cells and neurons [12].
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