Scientists find way to continue natural method to repair brains

 

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Scientists find way to continue natural method to repair brains

A team of Japanese and German scientists said its recent discoveries could lead to medicine that promotes and prolongs reparations to brain functions among victims of strokes and other diseases.

The researchers uncovered a mechanism that prompts recovery of brain functions in the early stages after the onset of the disease. They also identified a protein that causes the reparability to wane and eventually halt.

And they developed a drug that suppresses the workings of that protein in mice.

The group, including researchers from the Institute of Science Tokyo and the Tokyo Metropolitan Institute of Medical Science, plans to apply the findings to humans to ease the aftereffects of brain diseases.

Their research results were published online May 13 in Nature, a British science journal.

Infarction and other diseases of the brain cause neurological symptoms, such as loss of limb mobility and speech impairment.

Dead brain cells cannot be restored.

However, part of the lost brain functions can be recovered through rehabilitation, although the reparability is lost after a while. The science world does not understand exactly why this occurs.

The researchers on the team set their sights on microglia, a class of immune cells that work in the brain.

In mouse experiments, they found a mechanism whereby a brain injury prompts the microglia to begin generating nourishing substances that encourage brain tissue repair.

The microglia continued making the nourishing substances for about a month in mice that suffered a brain stroke. But production of the substances eventually stopped, and the reparative functions were lost in two months.

The researchers found that a protein called ZFP384 works to prevent the microglia from generating those nourishing substances.

In mice disabled from making ZFP384, the nourishing substances continued to be produced one month following the stroke, and the neurological symptoms improved, according to the team.

The researchers developed a drug that inhibits the workings of ZFP384 and administered it to mice one week and one month following the onset of a stroke.

They found the neurological symptoms improved and the brain functions continued to recover.

The scientists said the microglia-created nourishing substances encouraged the recovery of synaptic connections and other features of the nervous system.

SAME MECHANISM IN HUMANS?

Among humans with brain infarction, the scholars found abundant microglia of the type that generates the nourishing substances one week following the disease.

Similar microglia, however, decreased with time in terms of abundance, leading to a loss of reparative functions. The researchers also found that more ZFP384 was being generated.

The scientists said this likely represents the same sort of change that took place in mice, and they are hoping to develop therapeutic drugs that work in humans as well.

“We have presented this novel therapeutic concept of relying on the natural reparability that is inherent in the brain and making it last longer,” said Jun Tsuyama, a Science Tokyo junior associate professor of neuroscience, one of the leading members of the research team.

“We hope to help realize medical treatment where you don’t have to give up hopes for post-stroke functional recovery with no lingering aftereffects,” he said.

The research article can be viewed at (https://www.nature.com/articles/s41586-026-10480-0).