Researchers at Johns Hopkins University have identified more than 200 types of wrong proteins in mice that can be associated with age -related cognitive decline.

The results can lead the way to finding new therapeutic goals and treatments in humans that can provide comfort for millions of people over the age of 65 years who suffer from Alzheimer’s, dementia or other diseases that steal them from their memories and independence with their age.

“The amydids are the accumulation of Miskhapen proteins.” Our research shows that amyloids are only the tip of the iceberg. “

The results were published on July 11 in Science progress.

To understand the molecular differences between the ancient minds that are mentally acute and those that suffer from a decrease, a unique and his team studied the 17 -year -old mice that arose in the same colony. The performance of seven bad mice was in memory tests and problem solving and considered cognitive weakness, while 10 performance in addition to the 6 -month -old mice.

Then the researchers measured more than 2,500 types of protein in the hippocampus, which is part of the brain associated with spatial learning and memory. For the first time, scientists were able to identify a large number of proteins, whether individual proteins were incorrect or folded, which allowed researchers to identify the wrong proteins of all mice and are associated with aging in general against the wrong proteins specifically in poor mice.

More than 200 proteins have been explained in poor mice, but have maintained their shapes in cognitive health mice. The researchers said the results indicate that some of these proteins contribute to the cognitive decrease.

Unparalleled proteins cannot perform the tasks needed for a cell that works properly, so cells have a natural monitoring system that determines and destroys these wrong proteins. Previously, researchers believed that the wrong proteins-especially the A-Beta and Tau-were only troubled when they gathered in amydids.

Farid said: “We believe that there are many proteins that can be wrong, do not form amydids, and still are a problem,” Farid said. “This indicates that these wrong proteins have ways to escape from this monitoring system in the cell.”

But exactly how these unparalleled proteins through the cell security system remain a mystery.

After that, the team plans to consider the wrong proteins under the high -precision microscope to get a more detailed picture of what its distortions look at the molecular level.

“Many of us have suffered from a family member or a relative who has become less able to do these daily tasks that require cognitive abilities,” Farid said. “Understanding what is going on physically in the brain can lead to better treatments and preventive measures.”