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Towards Neuro-CoViD-19


Francesco Chiappelli



UCLA Center for the Health Sciences, Los Angeles, California, USA,



Francesco Chiappelli, - E-mail: Chiappelli.research@gmail.com


Article Type

Research Article



Received March 17, 2019; Accepted March 18, 2020; Published April 30, 2020



CoViD-19 is the current pandemic caused by the Severe Acute Respiratory Syndrome Corona Virus-2 (SARS-CoV-2). Infection by SARSCoV-2 occurs via the binding of its S protein to the angiotensin-converting enzyme-2 receptor (ACE2-R). S binding to ACE2-R leads to a drop in ACE2, a homolog of angiotensin converting enzyme (ACE). In the central nervous system (CNS), ACE mediates neuroinflammation, neurodegeneration and neurotoxicity responsible for several CNS disorders. ACE2 counteracts the damaging effects of ACE on CNS neurons. SARS-CoV-2 can directly access the CNS via the circulation or via cranial nerve I and the olfactory bulb. Inactivation of ACE2 following binding of SARS-CoV-2 S protein to ACE2-R in situ might blunt ACE2-moderating effects upon ACE CNS neurotoxicity and neurodegeneration. Here, we propose a neurobiological mechanism directly involving SARS-CoV-2 binding to ACE2-R in the etiology of putative Neuro-CoViD-19.



Angiotensin-converting enzyme-2 receptor (ACE2-R); Central Nervous System (CNS); Corona Virus Disease 2019 (CoViD-19); Severe Acute Respiratory Syndrome Corona Virus-2 (SARS-CoV-2); transmembrane protease serine-2 (TMPRSS2)



Chiappelli, 16(4): 288-292 (2020)


Edited by

P Kangueane






Biomedical Informatics



This is an Open Access article which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. This is distributed under the terms of the Creative Commons Attribution License.