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.
We are very pleased to announce that the BMBF has approved an increase of the funding of the company Tokeya Deep Data Dive GmbH & Co. KG for the financing of the IASON project. The new funds will be used to develop an app combining an automated olfactory and memory test, the two positive results of which allow to predict that people will NOT develop Alzheimer's disease with a probability of 96% within the next 4 years (see “Olfactory test” the study of Devanand et al). The olfactory test will also be used to clarify symptoms of COVID-19 odour loss.
Most importantly, we will use the financial increase to plan, prepare and conduct a pilot study called FHASE (Forty Hertz (40 Hz) Alzheimer Stimulation and Entrainment), which will make it possible to significantly increase the effect strength of a combined 40 Hz Gamma Entrainment (optical, acoustic, mechanical, electrical) using an individual setting compared to previous approaches to Gamma Entrainment. We hope to gain decisive impulses for a sustainable, non-invasive, non-drug therapy of Alzheimer's disease.
“Entrainment” here means “rhythmic coupling of brain waves in the gamma frequency range (40 Hz)” by external (sensory) or internal (e.g. electrodes in the brain) stimulation. Entrainment here has the figurative meaning of “getting back into a synchronously running train (of oscillations)”. It is precisely this synchronicity that is lost in Alzheimer’s disease. Gamma Entrainment restores a normal (“healthy”) synchronization of the brain waves and at the same time eliminates the causes (e.g. plaques or tangles) of their disruption by the microglia cells. To show this improvement for humans and not only for mice is the declared goal of the FHASE pilot study.
A further central goal is to use the accompanying measurements (especially EEG) during gamma entrainment in the waking and sleeping states to gain insights that allow a prognosis of the future manifestation of Alzheimer’s disease already in its preclinical phase or in the MCI precursor state.
Then it would also be possible to postpone or even prevent the future occurrence of Alzheimer's disease by an intervention with 40 Hz Gamma Entrainment. Details will be presented and continuously expanded in a separate sub-page of this project page www.iason.ai in the course of the project.
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 . 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.
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.
There was general agreement among the scientists that this would enable a “new era in Alzheimer's diagnosis” and that it is already being entered. This is because the data required to predict the future manifestation of Alzheimer's dementia can now be obtained easily from blood samples. As a result, cohort studies of AD disease are now possible for the first time, which allow changes in the relevant parameters of AD progression at close time intervals in a comparatively cost-effective manner. At the same time, examinations that are stressful for the patient, such as lumbar punctures and PET examinations with radioactive tracers, will increasingly fade into the background in the foreseeable future.
First reports on the new blood tests were published on the project homepage and on ALZFORUM. A short summary was written for the general public on the "End Alzheimer Now" platform. Further information can be found on this homepage under "Updates on the state of the art" under "Blood biomarker".
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).
The BO contains a large number of ACE2 receptors, which are known to be the entry point of the SARS CoV-2 virus into the cell. The distribution of the ACE2 receptors in mice and humans was recently examined in more detail by Chen et al (2020).
At the same time, the number of ACE2 receptors is reduced in Alzheimer’s disease, see the work of Kehoe et al (2016). Furthermore, Evans et al. (2020) could show that ACE2-enhancing activation helps in Alzheimer’s disease.
Thus, the replication pathway of the SARS CoV-2 virus via the ACE2 receptor and the protection against Alzheimer’s are in contrast to each other. It is therefore quite possible that COVID-19 promotes the risk of Alzheimer's. On the other hand, a deficiency of ACE2 receptors in existing Alzheimer’s disease may even be protective against COVID-19, especially in older patients with previous diseases, which is quite typical for Alzheimer's disease.
As was reported on March 11, 2020, a 100-year-old man in China with pre-existing conditions and Alzheimer's disease was able to recover from a COVID-19 disease, but only after receiving blood plasma from recovered COVID-19 patients as a transfusion, so that the antibodies contained in it apparently worked well. It is likely that this was the cause of his recovery. This is because in a similar case in Germany, in which a 33-year-old nurse without previous illnesses became ill with COVID-19 and almost died, the patient was also saved by a blood transfusion.