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WebMD on COVID-19 CNS symptoms

It's mainstream recognition that this is a danger to people, and that brainstem involvement may be one of the reasons people stop breathing. Personally, I suspect from what I have read that its a significant cause of mortality in COVID-19. If we can protect the brain, prevent apoptosis, far fewer people may die.

Neuroinfection may potentially contribute to pathophysiology and clinical manifestations of COVID-19.

Acta Physiol (Oxf). 2020 Mar 29:e13473. doi: 10.1111/apha.13473. [Epub ahead of print] Neuroinfection may potentially contribute to pathophysiology and clinical manifestations of COVID-19. Steardo L1,2, Steardo L Jr3, Zorec R4,5, Verkhratsky A5,6. Author information Abstract The new coronavirus, classified as SARS-CoV-2 that emerged in Hubei province in China, causes a new coronavirus disease, which was termed COVID-19 by WHO on February 11, 2020. COVID-19 claimed almost 19000 lives around the world by March 25, 2020. PMID: 32223077 DOI: 10.1111/apha.13473

Evidence of the COVID-19 Virus Targeting the CNS: Tissue Distribution, Host–Virus Interaction, and Proposed Neurotropic Mechanisms

The recent outbreak of coronavirus infectious disease 2019 (COVID-19) has gripped the world with apprehension and has evoked a scare of epic proportion regarding its potential to spread and infect humans worldwide. As we are in the midst of an ongoing pandemic of COVID-19, scientists are struggling to understand how it resembles and differs from the severe acute respiratory syndrome coronavirus (SARS-CoV) at the genomic and transcriptomic level. In a short time following the outbreak, it has been shown that, similar to SARS-CoV, COVID-19 virus exploits the angiotensin-converting enzyme 2 (ACE2) receptor to gain entry inside the cells. This finding raises the curiosity of investigating the expression of ACE2 in neurological tissue and determining the possible contribution of neurological tissue damage to the morbidity and mortality caused by COIVD-19. Here, we investigate the density of the expression levels of ACE2 in the CNS, the host–virus interaction and relate it to the pathogenesis and complications seen in the recent cases resulting from the COVID-19 outbreak. Also, we debate the need for a model for staging COVID-19 based on neurological tissue involvement. Keywords: Coronavirus, SARS-CoV-2, COVID-19, ACE2 tissue distribution, host−virus interaction, spike protein

The neuroinvasive potential of SARS-CoV2 may be at least partially responsible for the respiratory failure of COVID-19 patients

"The most characteristic symptom of COVID-19 patients is respiratory distress, and most of the patients admitted to the intensive care could not breathe spontaneously. Additionally, some COVID-19 patients also showed neurologic signs such as headache, nausea and vomiting. Increasing evidence shows that coronaviruses are not always confined to the respiratory tract and that they may also invade the central nervous system inducing neurological diseases. The infection of SARS-CoV has been reported in the brains from both patients and experimental animals, where the brainstem was heavily infected. Furthermore, some coronaviruses have been demonstrated able to spread via a synapse-connected route to the medullary cardiorespiratory center from the mechano- and chemoreceptors in the lung and lower respiratory airways".