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| Study reveals a new approach to Alzheimer's therapies |
Researchers hypothesize that Medin could be a therapeutic target to prevent vascular damage and cognitive loss as a result of amyloid deposition in the blood vessels of the brain. Germany's Berlin Along with the protein amyloid, the protein medin accumulates in the blood vessels of Alzheimer's sufferers' brains. This co-aggregation was identified by the DZNE team of researchers.
Since then, news of their discovery has appeared in the prestigious publication Nature. "Despite being used for more than 20 years, Medin's effect on ailments wasn't fully understood until recently. We were able to show that medin significantly speeds up the degenerative changes in Alzheimer's sufferers' blood vessels." Director of the DZNE's Tubingen division and study's lead investigator, Dr. Jonas Neher, claims.
The University of Tubingen, the Hertie Institute for Clinical Brain Research in Tubingen, as well as a number of international organizations and cooperation partners, participated in this extensive study as well.
An example of an amyloid is Medin. The most well-known of these proteins is amyloid, which clumps together in the brains of people with Alzheimer's disease. The following deposition of these aggregates as so-called plaques causes harm to the brain's blood vessels and tissue, as well as to the brain's nerve cells and blood vessels.
But although amyloid has been the focus of many studies, medin has not received much attention. There was no indication of pathology, or of a clinically significant finding associated with medin, according to Jonas Neher, who also points out that pathology is typically a need for a more thorough investigation of amyloid.
The most common amyloid, however, known as Medin, is found in the blood vessels of almost everyone over the age of 50. Neher and his colleagues discovered that medin even appears in aged mice, and they published their research on this two years ago in the academic journal PNAS.
At that time, it was shown that medin collected more in the brain blood vessels of the mice as they grew older. Additionally, as the brain becomes active and increases blood flow, medin-deposited blood vessels expand more slowly than medin-free blood vessels. However, for the brain to get the highest possible amount of oxygen and nutrients, the blood vessels' capacity to expand is essential.
On top of this framework, the researchers' most recent discoveries concentrated on Alzheimer's disease. First, they were able to show that the presence of amyloid deposits causes medin to concentrate substantially more firmly in the blood arteries of the brain in Alzheimer's mouse models.
Importantly, the examination of brain tissue from organ donors who had Alzheimer's disease validated these observations. However, animals whose genes were changed to prevent the production of medin had far fewer amyloid deposits, which led to fewer blood vessel damage.
According to Jonas Neher, there are very few research organizations working on medin in the entire world. Medin levels may rise in Alzheimer's sufferers, according to a new U.S. research. It is still not clear, though, whether this rise is only a side effect of the illness or if it is one of the reasons.
Through several trials, "we have now been able to demonstrate that medin really causes vascular disease in Alzheimer's models," stated Neher. Therefore, medin deposits are a factor in damaged blood vessels. And this shows that one of the diseases' causes is medin, according to Neher.
The researchers utilized tissue samples from mice and Alzheimer's patients that had been colored to make certain proteins visible. They were able to show that medin and amyloid- are deposited jointly in the blood vessels of the brain, or co-localized.
In a later stage, they were able to show that these two amyloids also co-aggregate, or form mixed deposits. According to Jonas Neher, the results. It is amazing to learn that medin interacts directly with amyloid and enhances its aggregation.
This finding gives the researchers hope for the development of a revolutionary therapy. They propose that Medin may be a therapeutic target to prevent vascular damage and cognitive loss as a result of amyloid deposition in the blood vessels of the brain.
In addition to amyloid aggregates in the brain tissue, vascular alterations, impaired function, or damage to blood vessels undoubtedly contribute to the development of Alzheimer's disease. Therefore, treatments that concentrate on both plaques and damaged blood vessels may be advantageous for patients.
The next aim is to find out if medin aggregates can be eliminated therapeutically and, if so, if doing so has any actual effects on cognitive performance. The researchers will initially test this in mice since they are an excellent representation of the pathogenic changes in Alzheimer's sufferers.
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