IASON is a joint project of Tokeya Deep Data Dive GmbH & Co. KG and the chair of clinical psychology and psychotherapy (KliPs) at the Friedrich-Alexander-University (FAU) Erlangen-Nuremberg.

The name “IASON” means “the healer” in Greek and is a heroic figure from Greek mythology.

On the one hand, the IASON project aims to develop a tool for the simple and rapid early diagnosis of Alzheimer's dementia. This tool will be based in particular on the analysis of data from electroencephalography (EEG) and other characteristic data, which are available in significantly altered form in Alzheimer's dementia.

The second focus of the IASON project is the development of an intelligent, emotional-empathetic digital assistant (IEEDA), which supports patients as well as their relatives and nursing staff in communicating with Alzheimer's patients in a variety of sensitive ways.

The IASON project is funded by the Federal Ministry of Education and Research (BMBF), see project description (BMBF), and was selected by the BMBF for the “Project Gallery 2019” alongside 13 other of the funded projects 2019 in the area of “Human-Technology Interaction”.

In the times of the COVID-19 crisis, the IASON project must also change. We will also make our contribution to support the dementia patients to be cared for in times of the threat of COVID-19! More about this under “The IASON project in times of the COVID-19 crisis”.

Due to the development of the COVID-19 crisis, we feel compelled to publish this project page currently in a temporary transition stage.

The project will undergo some structural changes due to the necessary measures to protect the patients, which can only be reported on at a later date, e.g. after the summer holidays 2020.

For this reason, the individual points of content, particularly with regard to the project structure, objectives and methods used, are only briefly presented here in a concise form and will be updated in a concrete manner at a later date.



Loss of sense of smell with COVID-19

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.

Participation in Conference on Alzheimer’s disease

The partners in the joint project IASON participated in the world’s largest conference on Alzheimer’s disease AAIC, which was originally planned to take place in Amsterdam from 27.7.-31.7.20, but which now had to be conducted virtually due to the COVID-19 pandemic. On 28.7.20 the Swedish research group around H. Zetterberg from the University of Gothenburg reported as a world novelty extraordinary progress in the development of blood tests for the very early diagnosis of Alzheimer’s disease.

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Sars-CoV-2 and Alzheimer’s dementia

It is now known that people suffering from COVID-19 temporarily lose their sense of smell and taste. This assumes that the viruses invade the olfactory bulb of the brain (Bulbus olfactorius = BO).

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