The SPIEGEL of 20.8.20 reported on a study on the loss of the sense of smell in COVID-19 diseases, in which the frequency of ACE2 receptors, which are used by the SARS-CoV-2 virus as entry port into the cell, was determined on the basis of human tissue, including the olfactory mucosa.

The authors of the study, Chen et al, write: “In the early stages of SARS-CoV-2 infection, viral RNA can easily be detected in upper respiratory tract samples, but not in blood, urine or stool [19]. These findings, together with the cellular localization of the ACE2 protein presented here, suggest that active viral infection and replication takes place in the apical (i.e. ‘uppermost, free’) layer of the nasal and olfactory mucosa”.

Another point is that ACE2 is apparently expressed differently in different populations, which could explain the different vulnerability in different countries. Similarly, children have a lower expression of ACE2 in the nasopharynx, which may explain the lower susceptibility in them. In particular, there is an inhibitor of ACE2 for the TMPRSS2 required by the virus, which could be used for medication during the course of the disease, especially prophylactically at the onset of anosmia, because it docks to ACE2, virtually occupies the receptor and thus SARS-CoV-2 “takes the place away”, similar to what the influenza virus would do, which uses the same ACE2 receptor (also via the spike protein).

On the other hand, blocking the ACE2 is also an intervention in the complex renin-angiotensin-aldosterone system (RAAS), in which, among other things, blood pressure is increased, e.g. by means of contraction of the blood vessels. Therefore, “contact sites to the outside” such as the lungs, intestines and olfactory system, but also the kidneys and the nervous system are particularly affected by COVID-19, in which many (small) blood vessels are inevitably involved, in the vicinity of which much ACE2 is expressed.

It is therefore certainly necessary to take advantage of the above-mentioned early signs of infection with SARS-CoV-2 already in the anamnesis of potential COVID-19 patients in order to be able to initiate a therapy appropriate to the individual situation of the patient, which does not burden either him or society as in the past.

Since Alzheimer's disease begins in the entorhinal cortex with the loss of the sense of smell and a p-tau deposition, the question arises whether COVID-19 also leads to an increased (p-)tau deposition due to the symptomatically occurring anosmia (if neurological symptoms are present) and whether this can therefore be measured with one of the mentioned blood tests and used to diagnose COVID-19.