Possible new therapeutic goal – healing practice

Dementia: connection between protein and Alzheimer’s discovered

disease Alzheimer cannot be cured yet. However, especially in the early and middle stages, drugs and non-drug treatment methods can help to maintain memory performance for as long as possible and to alleviate side effects. Researchers now have a new one starting point for Alzheimer’s therapies found.

Alzheimer is the most common form of dementia. The treatment of this disease, which has not yet been cured, is stagnating despite the great increase in knowledge in recent years and the development of new drugs. Now researchers have discovered a new potential therapeutic target. Their study results were published in the journal “Nature” released.

Influence has been underestimated so far

As in a current Message of the German Center for Neurodegenerative Diseases (DZNE), the protein Medin is also deposited in the blood vessels of the brain of Alzheimer’s patients together with the protein amyloid-β. Scientists at the DZNE discovered this so-called co-aggregation.

“Although Medin has been known for around 20 years, its influence on diseases has been underestimated so far. We were able to show that pathological changes in the blood vessels of Alzheimer’s patients are significantly increased by Medin”explains the head of the study dr Jonas Neher from the Tübingen site of the DZNE.

At the long-term study The Hertie Institute for Clinical Brain Research in Tübingen, the University of Tübingen and other international institutions and cooperation partners were also involved.

Aggregates are also deposited in blood vessels

According to the information, Medin belongs to the group of amyloids. Of these proteins, amyloid-β is best known because it clumps together in the brains of people with Alzheimer’s disease. These aggregates are then deposited as so-called plaques directly in the brain tissue, but also in its blood vessels, thereby damaging the brain Neurons or the blood vessels.

Therefore, while many studies have dealt with amyloid-β, Medin has not been the focus of interest so far. “There was little evidence of pathology, i.e. of a clinically conspicuous finding in connection with Medin – and that is often the prerequisite for a more detailed study of an amyloid”according to Neher.

In fact, Medin is found in the blood vessels of almost everyone over the age of 50, making it the most common amyloid known. Neher and his team originally found that Medin even develops in aging mice, and reported two years ago in the journal “PNAS‘ about this discovery.

The older they get, the more Medin accumulates in the blood vessels of the brains of mice – that was the finding at the time. And when the brain becomes active and more blood supply required, vessels with Medin deposits expand more slowly than those without Medin.

This ability of expansion is important in order to get the most out of the brain oxygen and supply nutrients.

Only a few researchers are working on Medin

For your recent results The researchers built on this foundation and looked specifically at Alzheimer’s disease.

Using Alzheimer’s mouse models, they were able to show that Medin accumulates even more in the blood vessels of the brain if amyloid-β deposits are also present there. Corresponding findings could then also be brain tissue detected by organ donors with Alzheimer’s dementia.

However, if mice were genetically modified in such a way that Medin could not be formed, there were significantly fewer amyloid β deposits and thereby significantly less damage to the blood vessels.

“There are only a handful of working groups worldwide that work on Medin at all”, explains Neher. A previous study from the USA recently described that the level of medicine in Alzheimer’s patients increases. However, it remained unclear whether this is only the consequence of the disease or whether it is one of the causes heard.

“We have now been able to show in many experiments that Medin promotes vascular pathology in Alzheimer’s models”, says Neher. So the Medin deposits are actually a cause of the damage of blood vessels. “And that is an indication that it is one of the causes of the disease”according to the scientist.

Hope for the development of a possible therapy

In their studies, the researchers stained tissue sections from both mice and Alzheimer’s patients in such a way that specific proteins became visible. This enabled them to show that Medin and amyloid-β are deposited together in the blood vessels of the brain – co-localization is the technical term for it.

With further experiments, the experts were able to prove in a next step that these two amyloids also co-aggregate – that is mixed clusters form. “Amazingly, Medin interacts directly with amyloid-β and promotes its aggregation – this was completely unknown at that time”says Neher.

This is exactly what the researchers draw on Hope for the development of a possible therapy. “Medin could be a therapeutic target to prevent vascular damage and cognitive decline resulting from amyloid accumulation in the blood vessels of the brain,” they conclude.

In expert circles, it is undisputed that the causes of Alzheimer’s disease are not only the aggregates of amyloid-β in the brain tissue, but also vascular changes – i.e. the reduced function or the damage of blood vessels.

So if during a treatment not only the plaques than attackpoint are taken, but also the affected blood vessels, this could help the patients.

In a next step, it must now be clarified whether Medin aggregates that have already formed can be removed therapeutically and whether this intervention actually has an impact on the memory performance Has.

The scientists first want to test this on mouse models, since these are the pathological ones changes reflected very well in Alzheimer’s patients. (ad)

Author and source information

This text corresponds to the requirements of medical specialist literature, medical guidelines and current studies and has been checked by medical professionals.


  • German Center for Neurodegenerative Diseases: New starting point for Alzheimer’s therapies found, (accessed: November 19, 2022), German Center for Neurodegenerative Diseases
  • Jessica Wagner, Karoline Degenhardt, Marleen Veit, Nikolaos Louros, Katerina Konstantoulea, Angelos Skodras, Katleen Wild, Ping Liu, Ulrike Obermüller, Vikas Bansal, Anupriya Dalmia, Lisa M. Häsler, Marius Lambert, Matthias De Vleeschouwer, Hannah A. Davies, Jillian Madine, Deborah Kronenberg-Versteeg, Regina Feederle, Domenico Del Turco, K Peter R Nilsson, Tammaryn Lashley, Thomas Deller, Marla Gearing, Lary C Walker, Peter Heutink, Frederic Rousseau, Joost Schymkowitz, Mathias Jucker & Jonas J Neher: Medin co-aggregates with vascular amyloid-β in Alzheimer’s disease; in: Nature, (published: 2022-11-16), Nature
  • Karoline Degenhardt, Jessica Wagner, Angelos Skodras, Michael Candlish, Anna Julia Koppelmann, Katleen Wild, Rusheka Maxwell, Carola Rotermund, Felix von Zweydorf, Christian Johannes Gloeckner, Hannah A. Davies, Jillian Madine, Domenico Del Turco, Regina Feederle, Tammaryn Lashley , Thomas Deller, Philipp Kahle, Jasmin K. Hefendehl, Mathias Jucker & Jonas J. Neher: Medin aggregation causes cerebrovascular dysfunction in aging wild-type mice; in: PNAS, (published: 08.09.2020), PNAS

Important NOTE:
This article contains general advice only and should not be used for self-diagnosis or treatment. He can not substitute a visit at the doctor.

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