A new study has found that removing a certain protein in the brain could help reduce the damage caused by Alzheimer’s disease.
The research was published in the journal eNeuro and was led by Dr. Erzsebet Szatmari and her team.
They focused on a protein called Centaurin-α1. This protein is found in high amounts in the brains of people with Alzheimer’s disease. Earlier studies suggested that it might play a role in the damage seen in the disease. To find out more, the researchers removed this protein in mice that had been specially bred to show signs of Alzheimer’s disease.
These mice, known as the J20 model, carry two genetic changes found in rare inherited forms of Alzheimer’s. The mice develop many of the same brain problems seen in humans, including inflammation, buildup of harmful plaques, loss of connections between brain cells, and trouble with memory and learning.
When the scientists removed Centaurin-α1 from the mice, they noticed some important changes. First, there was much less inflammation in the brain. Inflammation is one of the early signs of Alzheimer’s and can make the disease worse. In the mice without the protein, the usual signs of inflammation were not present.
Second, the researchers saw fewer amyloid plaques. These plaques are sticky clumps that build up between brain cells and are a well-known sign of Alzheimer’s. In one key area of the brain called the hippocampus, which is important for memory, the number of plaques dropped by about 40%.
However, this change wasn’t seen in another brain area called the neocortex. This suggests that the plaques might behave differently in different parts of the brain, and treatments may need to work in more than one way.
The team also found that removing Centaurin-α1 helped protect brain cell connections in the hippocampus. This is important because these connections are needed for learning and memory. Mice without the protein performed better on tests that measured spatial learning, which is often a problem in Alzheimer’s.
Dr. Szatmari said that the improvements in memory and brain health show that Centaurin-α1 might be a good target for future treatments. However, more work is needed to understand exactly how this protein affects the disease.
To learn more, the researchers looked at gene activity in the brains of healthy mice, diseased mice, and diseased mice without Centaurin-α1. In the diseased mice, many genes were either too active or not active enough. But in the mice without Centaurin-α1, the levels of these genes were closer to normal.
Dr. Ryohei Yasuda, the senior author of the study, explained that Centaurin-α1 may affect many different brain functions. It seems to influence how cells communicate, which can impact inflammation, metabolism, plaque buildup, and brain cell connections. All of these are key problems in Alzheimer’s.
The researchers now want to find out if lowering Centaurin-α1 in adult brains, instead of removing it from birth, could still help. They also recently found that removing this protein helped in mice with multiple sclerosis, another brain disease.
This suggests that Centaurin-α1 might be involved in several brain conditions and could be a useful target for future treatments.
