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Last Updated: Monday, 14 November 2005, 00:07 GMT
Stroke 'cell-death trigger' found
Disability after stroke is caused by brain cell death
Identifying a signal in brain cells that tells them to die after a stroke could help prevent stroke-induced disability and deaths, scientists say.

German and Italian teams found that in mice they could control a protein trigger for cell death, which leads to stroke damage.

In Nature Medicine, they said it was possible to block this switch, raising hopes a drug could do the same.

UK experts said a potentially "very important discovery" had been made.

Strokes lead to death or permanent disabilities for millions globally.

If the mechanism demonstrated in this research in mice is shown to be similar in humans then we have the possibility of developing drugs that might begin to make a real difference
Dr Tony Rudd, Guy's and St Thomas' Hospital, London

They occur when the flow of blood to the brain is interrupted, depriving brain cells of vital oxygen and nutrients.

This can lead to damage and even cell death. Once cells die, they cannot recover, but damaged cells can.

So preventing cell death can reduce the effects of a stroke, such as paralysis and speech impairment.

'Promising findings'

Researchers from the University of Heidelberg and the University of Ulm looked at what happened next in brain cells.

They created a stroke-like condition in mice, and focused on an internal cell communications network called NF-kB.

This comes into play when cells in the brain are damaged, triggering the cells to self-destruct.

A protein called IKK2, was found to activate NF-kB.

In mice with an over-active form of IKK2 in neurons, and therefore too much NF-kB signalling, far more cells died.

But if the IKK2 signal was blocked, damaged cells stayed alive and appeared to show signs of recovery.

Damaged tissues were still alive several days after the stroke.

The researchers said their findings were promising in terms of implications for the treatment of stroke in humans in two ways.

Shutting down the IKK2 signal had beneficial effects even when it was done a few hours after the stroke, which is important because it usually takes time for a patient to reach hospital.

In addition, researchers were able to block IKK2 activity with a small artificial molecule, which is what a drug would need to do.

'Lack of treatments'

Dr Tony Rudd, a stroke specialist at Guy's and St Thomas' Hospital, London, said: "This is potentially an extremely important discovery.

"Understanding what happens to brain cells after the blood supply is cut off is vital if we are to develop effective treatments for stroke. "

He added: "Apart from clot-busting drugs, we have virtually nothing to limit the size of a stroke.

"If the mechanism demonstrated in this research in mice is shown to be similar in humans, then we have the possibility of developing drugs that might begin to make a real difference.

"There is still a long way to go but there is reason to be optimistic."

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