Abstract
The current pandemic caused by the new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a public health emergency. To date, March 1, 2021, coronavirus disease 2019 (COVID-19) has caused about 114 million accumulated cases and 2.53 million deaths worldwide. Previous pieces of evidence suggest that SARS-CoV-2 may affect the central nervous system (CNS) and cause neurological symptoms in COVID-19 patients. It is also known that angiotensin-converting enzyme-2 (ACE2), the primary receptor for SARS-CoV-2 infection, is expressed in different brain areas and cell types. Thus, it is hypothesized that infection by this virus could generate or exacerbate neuropathological alterations. However, the molecular mechanisms that link COVID-19 disease and nerve damage are unclear. In this review, we describe the routes of SARS-CoV-2 invasion into the central nervous system. We also analyze the neuropathologic mechanisms underlying this viral infection, and their potential relationship with the neurological manifestations described in patients with COVID-19, and the appearance or exacerbation of some neurodegenerative diseases.
Highlights
Coronavirus disease 2019 (COVID-19) was first reported in December 2019 in Wuhan, in Hubei province, China [1]
The underlying mechanism of brain abnormalities detected through neuroimaging remains to be understood, these findings provide further evidence that central nervous system (CNS) damage can occur in COVID-19 patients
Produces GBPA, that inhibits many of the serine proteases that SARS CoV and SARS-CoV-2 use for virus-to-host cell membrane fusion, like TMPRSS2**
Summary
Coronavirus disease 2019 (COVID-19) was first reported in December 2019 in Wuhan, in Hubei province, China [1]. Nucleus accumbens; ACC, anterior cingulate cortex; ACE2, angiotensin-converting enzyme 2; Amg, amygdala; ATR1, angiotensin receptor type 1; BBB, blood-brain barrier; BECs, brain endothelial cells; Cat, cathepsin; Cb, cerebellum; Cd, caudate nucleus; DPP4, dipeptidyl peptidase-4; FroCx, frontal cortex; HiF, hippocampal formation; Hy, hypothalamus; ITGB1, integrin subunit beta 1; KGE, Lys-Gly-Glu; MAPK, Mitogen-Activated Protein Kinases; MERS-CoV, Middle East Respiratory Syndrome Coronavirus; MI3K, myo-inositol 3-kinase; MMPs, matrix metalloproteinases; NF-kB, nuclear factor kappa B; NLRP3, nucleotide-binding domain-, leucine-rich repeat-containing receptor, pyrin domain-containing 3; OLGs, oligodendrocytes; PG, pituitary gland; Pu, putamen; RGD, Arg-Gly-Asp; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; SC, spinal cord (cervical c-1), SN, substantia nigra; TLR, Toll Like Receptor; TMPRSS2, transmembrane protease serine 2.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
