Saturday , July 24 2021

Researchers have discovered a brain section that appears to be "neutral" for Alzheimer's disease

As part of the collection of the largest ever possible human brain map under the influence of Alzheimer's disease, researchers found more evidence that part of our brain could actually be protected from the devastating effects of the disease.

The team found that the brain – the part of the brain responsible for movement and balance – is undergoing an important but subtle change due to Alzheimer's disease, which may be a sign that the brain is trying to put up defense.

This is important because the brain, in addition to regions such as motorcycle and sensory bark, is suspected of being not worn by the disease as other brain regions. But nobody is sure why.

In this study, the group found that cerebellum passed through additional changes after Alzheimer's stroke, which did not reflect in the motor and sensory crust.

In other words, something unique in cerebellum appears, scientists say, that this could help develop a treatment that imitates this behavior.

"The little brain had previously thought." [to] without affecting treatment, shows an important response at the molecular level, "says Richard Unwin, lead researcher at the University of Manchester in the UK.

"Many changes are not visible here in other regions, and this can mean that this region is actively protected against diseases. We will not surely know until we carry out more research."

Obviously, the little man is not unique because it is altered by Alzheimer's disease, but it changes in a way that is different from other regions of the brain – especially when accumulating amyloid and tau, which indicates disease in most other parts of the brain.

For now, this is just a hypothesis, but researchers think that the "little brain" brain cells can have survival mechanisms that the rest of the brain does not have.

For the study, scientists looked at nine people who died with Alzheimer's and nine healthy brains, from people who died of other causes, including heart disease, pulmonary disease and cancer.

They succeeded in mapping 5,825 types of proteins in six different regions of the brain, giving them 24,024 data points – and a treasure trove of information for researchers who want to track the progress of Alzheimer's disease. The data is now publicly available.

alz 2(University of Manchester)

"This database offers an excellent opportunity for researchers with dementia around the world to advance and monitor new areas of biology and develop new treatments," says Unwin.

"This could also help to confirm observations in animal or cellular disease models in humans. It is very exciting to publish this information so that scientists can access and use these important information."

The study was carefully studied by the entorchinal cortex, the cingular gyrus and the hippocampus, where Alzheimer's disease should begin. We already know that these brain regions tend to have Alzheimer's disease.

In other regions where the main surprise was found: motor crust and sensory crust remained largely untouched, as expected, but the small brain showed a different pattern of changes in proteins that could be protective.

Unfortunately, despite many recent advances in our understanding, Alzheimer's disease remains incurable. In the past year, researchers have discovered a range of immunity against Alzheimer's disease in some people, as well as a potentially crucial link to gum disease.

All this brings us closer to overcoming Alzheimer's disease, as well as 44 new protein changes found by this latest study. The team could also point out relatively early and relatively late changes in the expression of proteins in damaged brain – again useful knowledge for work on treatment in the future.

"We believe that the changes we see in the affected regions represent early changes in the disease that are present before cells die," says Unwin. "These are good new targets for drug developers, because we know it's important to try to mediate early."

The research was published in 2006. T Communication biology.

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