Dementia: Link between protein and Alzheimer’s discovered
Illness Alzheimer’s can’t be cured yet. However, especially in the early and middle stages, pharmacological and non-pharmacological treatment methods can help maintain memory performance for as long as possible and alleviate side effects. The researchers now have a new one. point by alzheimer therapies found.
Alzheimer’s is the most common form of dementia. The treatment of this disease, which still has no cure, has stagnated despite the great increase in knowledge in recent years and the development of new drugs. Now the researchers have discovered a new potential therapeutic target. The results of their study were published in the journal Nature.
The influence has been underestimated so far.
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 brain of Alzheimer’s patients together with the amyloid-β protein. The DZNE scientists discovered this so-called coaggregation.
“Although Medin has been known for about 20 years, its influence on disease has so far been underestimated. We were able to show that Medin significantly increases pathological changes in the blood vessels of Alzheimer’s patients.”explains study leader Dr. Jonas Neher from the Tübingen site of the DZNE.
In the long term study The Hertie Institute for Clinical Brain Research in Tübingen, the University of Tübingen and other international institutions and cooperation partners also participated.
Aggregates are also deposited in blood vessels.
According to the information, Medin belongs to the group of amyloids. Of these proteins, amyloid-β is the 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, thus damaging the brain. neurons or 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, that is, 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 aged mice and reported their discovery two years ago in the journal PNAS.
The older they get, the more Medin 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 Blutzufuhr required, vessels with medin deposits expand more slowly than those without medin.
This expandability is important to get the most out of the brain. oxygen and supply nutrients.
Only a few researchers are working in Medin
For you recent results The researchers built on this foundation and looked specifically at Alzheimer’s disease.
Using mouse models of Alzheimer’s, they were able to show that Medin accumulates further in brain blood vessels if amyloid-β deposits are also present. The corresponding findings could also be brain tissue detected by organ donors with Alzheimer’s dementia.
However, if the mice were genetically modified in such a way that Medin could not form, there would be significantly fewer β amyloid deposits and therefore significantly less damage to blood vessels.
“There are only a handful of task forces in the entire world working on Medin”Neher explains. An earlier US study recently reported that the drug level in Alzheimer’s patients is increased. However, it was not clear if this is only the consequence of the disease or if it is one of the Causes Heard.
“We have now been able to demonstrate 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 in the development of a possible therapy.
In their studies, the researchers stained sections of tissue from both mice and Alzheimer’s patients in such a way that specific proteins became visible. This allowed them to show that Medin and amyloid-β are deposited together in the blood vessels of the brain. colocalization is the technical term for it.
With further experiments, the experts were able to prove in the next step that these two amyloids also co-aggregate, i.e. mixed bunches the picture. “Surprisingly, Medin directly interacts with amyloid-β and promotes its aggregation; this was completely unknown at the time.”Neher says.
This is exactly what the researchers are relying on. Expect for the development of a possible therapy. “Medin could be a therapeutic target to prevent vascular damage and cognitive impairment resulting from the accumulation of amyloid in the blood vessels of the brain,” they conclude.
In expert circles, it is indisputable that the causes of Alzheimer’s disease are not only β-amyloid aggregates in brain tissue, but also vascular changes, i.e. reduced function or damage of blood vessels.
So if during a treatment not only the plates that point of attack are taken, but also the affected blood vessels, this could help patients.
In a next step, it now needs to be clarified whether the Medin aggregates that have already formed can be removed therapeutically and whether this intervention actually has an impact on the memory performance hat.
The scientists first want to test this in mouse models, since these are the pathological ones. changes reflects very well on Alzheimer’s patients. (ad)
Author and source of information
This text meets the requirements of specialized medical literature, medical guidelines, and current studies and has been reviewed by medical professionals.
- German Center for Neurodegenerative Diseases: A 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 coaggregates with vascular amyloid-β in Alzheimer’s disease; In: Nature, (published: 11.16.2022), 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 Feederle, Tammaryn Lashley , Thomas Deller, Philipp Kahle, Jasmin K. Hefendehl, Mathias Jucker, and Jonas J. Neher: Medin aggregation causes cerebrovascular dysfunction in aging wild-type mice; In: PNAS, (published: 09.08.2020), PNAS
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