TY - JOUR
T1 - Putative mechanism of neurological damage in covid-19 infection
AU - Bandala, Cindy
AU - Cortes-Altamirano, José Luis
AU - Reyes-Long, Samuel
AU - Lara-Padilla, Eleazar
AU - Ilizaliturri-Flores, Ian
AU - Alfaro-Rodríguez, Alfonso
N1 - Publisher Copyright:
© 2021, Nencki Institute of Experimental Biology. All rights reserved.
PY - 2021
Y1 - 2021
N2 - The recent pandemic of the coronavirus infectious disease 2019 (COVID-19) has affected around 192 countries, and projections have shown that around 40% to 70% of world population could be infected in the next months. COVID-19 is caused by the virus SARS- CoV-2, it enters the cells through the ACE2 receptor (angiotensin converting enzyme 2). It is well known that SARS-CoV-2 could develop mild, moderate, and severe respiratory symptoms that could lead to death. The virus receptor is expressed in different organs such as the lungs, kidney, intestine, and brain, among others. In the lung could cause pneumonia and severe acute respiratory syndrome (SARS). The brain can be directly affected by cellular damage due to viral invasion, which can lead to an inflammatory response, by the decrease in the enzymatic activity of ACE2 that regulates neuroprotective, neuro-immunomodulatory and neutralizing functions of oxidative stress. Another severe damage is hypoxemia in patients that do not receive adequate respiratory support. The neurological symptoms that the patient presents, will depend on factors that condition the expression oACE2 in the brain such as age and sex, as well as the mechanism of neuronal invasion, the immune response and the general state of the patient. Clinical and histopathological studies have described neurological alterations in human patients with COVID-19These conditions could have a possible contribution to the morbidity and mortality caused by this disease and may even representhe onset of neurodegenerative activity in recovered patients.
AB - The recent pandemic of the coronavirus infectious disease 2019 (COVID-19) has affected around 192 countries, and projections have shown that around 40% to 70% of world population could be infected in the next months. COVID-19 is caused by the virus SARS- CoV-2, it enters the cells through the ACE2 receptor (angiotensin converting enzyme 2). It is well known that SARS-CoV-2 could develop mild, moderate, and severe respiratory symptoms that could lead to death. The virus receptor is expressed in different organs such as the lungs, kidney, intestine, and brain, among others. In the lung could cause pneumonia and severe acute respiratory syndrome (SARS). The brain can be directly affected by cellular damage due to viral invasion, which can lead to an inflammatory response, by the decrease in the enzymatic activity of ACE2 that regulates neuroprotective, neuro-immunomodulatory and neutralizing functions of oxidative stress. Another severe damage is hypoxemia in patients that do not receive adequate respiratory support. The neurological symptoms that the patient presents, will depend on factors that condition the expression oACE2 in the brain such as age and sex, as well as the mechanism of neuronal invasion, the immune response and the general state of the patient. Clinical and histopathological studies have described neurological alterations in human patients with COVID-19These conditions could have a possible contribution to the morbidity and mortality caused by this disease and may even representhe onset of neurodegenerative activity in recovered patients.
KW - ACE2 activity
KW - Brain
KW - COVID-19
KW - Neurological damage
KW - SARS-CoV-2
UR - http://www.scopus.com/inward/record.url?scp=85103894436&partnerID=8YFLogxK
U2 - 10.21307/ane-2021-008
DO - 10.21307/ane-2021-008
M3 - Artículo
C2 - 33949163
AN - SCOPUS:85103894436
SN - 0065-1400
VL - 81
SP - 69
EP - 79
JO - Acta Neurobiologiae Experimentalis
JF - Acta Neurobiologiae Experimentalis
IS - 1
ER -