For Alzheimer's Disease 'Cancer-promoting' Protein Holds Promise: Danish Scientists

A harmful protein that is known to spread cancer cells around the body could hold the key to allowing the brain to repair itself finds Danish scientists.

A "harmful" protein that is known to spread cancer cells around the body could hold the key to allowing the brain to repair itself finds Danish scientists.

The finding is a potentially significant breakthrough in the treatment of severe brain injuries and could help those suffering from neurodegenerative disorders, such as Alzheimer's disease, said the scientists at the University of Copenhagen.

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They found that the protein S100A4 plays a crucial role in brain protection and repair.

Scientists have known the protein as a key factor in metastasis, or the spread of cancer. It is not found in the brains of healthy individuals.

"This protein is not normally in the brain, only when there's trauma or degeneration," the Daily Express quoted lead researcher Oksana Dmytriyeva as saying.

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"When we deleted the protein in mice, we discovered their brains were less protected and less able to resist injury. We were surprised to find this protein in this role as we thought it was purely a cancer protein.

"We are very excited and hope the finding will eventually benefit people who need treatment for neurodegenerative disorders like Alzheimer's, though obviously we have a long way to go," Dmytriyeva added.

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The scientists also found the protein "activates" previously disabled signalling pathways in the brain.

Advanced tests are now being carried out in the light of the breakthrough, with those involved in the research convinced this will benefit Alzheimer's sufferers within years rather than decades.

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The Danish scientists are confident they can effectively turn the "previously underrated" S100A4 from a tumour-promoter into a multi-functioning -protein, which provides a "therapeutic" effect on the central nervous system.

Their findings appeared this week in the journal Nature Communications.

Source-ANI