Abstract
The whole world is suffering from the coronavirus disease 2019 (COVID-19) pandemic, induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) through angiotensin-converting enzyme 2 (ACE2). Neurological manifestations in COVID-19 patients suggested the invasion of SARS-CoV-2 into the central nervous system. The present study mapped the expression level of ACE2 in 12 brain regions through immunohistochemistry and detected ACE2 in endothelial cells and non-vascular cells. The comparison among brain regions found that pons, visual cortex, and amygdala presented a relatively high level of ACE2. In addition, this study demonstrates that the protein level of ACE2 was downregulated in the basal nucleus, hippocampus and entorhinal cortex, middle frontal gyrus, visual cortex, and amygdala of the brain with Alzheimer’s disease (AD) pathology. Collectively, our results suggested that ACE2 was expressed discriminatorily at different human brain regions, which was downregulated in the brain with AD pathology. This may contribute to a comprehensive understanding of the neurological symptoms caused by SARS-CoV-2 and provide clues for further research on the relationship between COVID-19 and AD.
Highlights
From December 2019, novel coronavirus disease 2019 (COVID-19) characterized by respiratory failure has become a global and historical disaster (Guan et al, 2020)
The renin–angiotensin system (RAS) is classically seen as an enzymatic cascade, in which angiotensinogen is cleaved by renin to release angiotensin I (Ang I)
A clear positive signal was detected in the slice stained by the angiotensin-converting enzyme 2 (ACE2) antibody, while there was no signal in the slice stained by the buffer
Summary
From December 2019, novel coronavirus disease 2019 (COVID-19) characterized by respiratory failure has become a global and historical disaster (Guan et al, 2020). Recent studies detected ACE2 in the rodent brain, mainly located in the neural cells, and simulated the process of SARS-CoV2 infection in human brain organoids (Doobay et al, 2007; Song et al, 2021). In the brain with AD pathology, the broken blood–brain barrier and dysregulated immune environment reflect a higher risk of virus infection and tissue damages. It is still controversial whether the distribution of ACE2, the receptor of SARS-CoV-2, was altered among AD pathology (Kehoe et al, 2016; Lim et al, 2020). We systemically compared the ACE2 expression in 12 brain regions in the brains comprising AD-related pathology or not
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