Journal
ACTA NEUROBIOLOGIAE EXPERIMENTALIS
Volume 81, Issue 1, Pages 69-79Publisher
NENCKI INST EXPERIMENTAL BIOLOGY
DOI: 10.21307/ane-2021-008
Keywords
SARS-CoV-2; COVID-19; ACE2 activity; brain; neurological damage
Categories
Ask authors/readers for more resources
The recent COVID-19 pandemic caused by SARS-CoV-2 has affected many countries and could potentially infect a significant portion of the world population. The virus enters cells through the ACE2 receptor and can cause respiratory and neurological symptoms, with potential long-term consequences for patients.
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 of ACE2 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-19. These conditions could have a possible contribution to the morbidity and mortality caused by this disease and may even represent the onset of neurodegenerative activity in recovered patients.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available