A possible new therapeutic target – healing practice

Dementia: link discovered between protein and Alzheimer’s disease

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

Alzheimer’s disease is the most common form of dementia. Despite the great increase in knowledge in recent years and the development of new drugs, the treatment of this still incurable disease is stagnant. Now scientists have discovered a new potential therapeutic target. The results of their study were published in the journal Nature.

The impact has so far been underestimated

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

“Although Medin has been known for around 20 years, its effect on diseases has been underestimated until now. We were able to prove that pathological changes in the blood vessels of patients with Alzheimer’s disease are significantly increased by Medin”, explains study leader Dr. Jonas Neher from the DZNE location in Tübingen.

IN 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 information, Medin belongs to the group of amyloids. Of these proteins, amyloid-β is the best known because it accumulates 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, thus damaging the brain Neurons or blood vessels.

Therefore, while many studies have looked at amyloid-β, Medin has not been a focus until now. “There was little evidence of pathology, that is, of a clinically striking finding in connection with Medin – and this is often a prerequisite for a more detailed study of 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 discovered that Medin even develops in aging mice and reported the discovery two years ago in the journal PNAS.

The older they get, the more Medina accumulates in the blood vessels of the mice’s brains – that was the finding at the time. And when the brain becomes active and more Blutzuführer Vessels with Medina deposits dilate more slowly than vessels without Medina.

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

Only a few researchers work on Medina

For you recent results Scientists built on this foundation and focused specifically on Alzheimer’s disease.

In mouse models of Alzheimer’s disease, they were able to demonstrate 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 organ donors with Alzheimer’s dementia.

However, if the mice were genetically modified so that Medin could not be produced, there were significantly fewer of them amyloid β deposit and thus significantly less damage to blood vessels.

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

“We have now been able to demonstrate in multiple experiments that Medin promotes vascular pathology in models of Alzheimer’s disease.”, says Neher. So the medina bearings are actually the cause damage blood vessels. “And this is a sign 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 patients with Alzheimer’s disease in such a way that specific proteins were visible. This allowed them to show that medin and amyloid-β are deposited together in the blood vessels of the brain – common localization there is a technical term for it.

Through further experiments, the experts were able to demonstrate in the next step that these two amyloids also aggregate together – i.e. mixed clusters picture. “It’s amazing that Medin interacts directly with amyloid-β and promotes its aggregation – this was completely unknown at the time”says Neher.

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

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

So if during treatment not only plaques than attack point they take, but also affected vessels, this could help patients.

In the next step, it is now necessary to clarify whether already formed Medina aggregates can be therapeutically removed and whether this intervention really has an effect on memory performance cap.

The researchers want to test it in mouse models first because those are the pathological ones Changes is very well reflected in patients with Alzheimer’s disease. (advertisement)

Author and source information

This text meets the requirements of the medical literature, medical guidelines and current studies and has been reviewed by health professionals.

Sources:

  • German Center for Neurodegenerative Diseases: A new starting point for the treatment of Alzheimer’s disease found, (Accessed: 19 November 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 De Viesle, Hanwerh A. Matthias, 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: 16/11/2022), 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 Lashley, Tammaryn , 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. It cannot replace a doctor’s visit.

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