Researchers have discovered the mechanism linked to stroke damage and brain function, thus paving the way to develop a new drug target to block brain damage.
Strokes happen when the blood supply to a part of the brain is cut off, but much of the harm to survivors' memory and other cognitive function is often actually caused by "oxidative stress" in the hours and days after the blood supply resumes.
The researchers studied the second phase of damage in laboratory mice and found a mechanism in neurons that, if removed, reduced the damage to brain function.
"This study has pinpointed a very promising drug target," said study co-author Lin-Hua Jiang from University of Leeds in Britain.
The study looked at the damage caused by the excessive production of chemicals called "reactive oxygen species" in brain tissues immediately after blood supply is re-established.
In a healthy brain, there are very low levels of reactive oxygen species, but the quantity dramatically increases after a stroke to levels that are harmful to neurons.
"We identified an 'ion channel' in the membranes of neurons, called TRPM2, which is switched on in the presence of the reactive oxygen species," Jiang added.
"We are now screening a large chemical library to find ways of effectively inhibiting this channel," Jiang said.
The study was published in the journal Cell Death and Disease.
