A mechanism that is linked with brain damage caused after a person suffers from a stroke has been identified by researchers, who are now analyzing ways through which it can be blocked.
Strokes happen when the blood supply to 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.
A team from the University of Leeds and Zhejiang University in China studied this second phase of damage in laboratory mice and found a mechanism in neurons that, if removed, reduced the damage to brain function.
The study, published in the journal Cell Death and Disease and supported by a strategic partnership between the University of Leeds and Zhejiang University, 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.
Dr Jiang said: "We identified an 'ion channel' in the membranes of neurons, called TRPM2, which is switched on in the presence of the reactive oxygen species. Basically, an ion channel is a door in the membrane of a cell that allows it to communicate with the outside world-- TRPM2 opens when the harmful levels of reactive oxygen species are present and we found that removing it significantly reduced neuronal cell damage."
The researchers compared the effects of strokes on mice with TRPM2 with a transgenic strain without it.
"In the mice in which the TRPM2 channel does not function, the reactive oxygen species are still produced but the neurons are very much protected. The neuronal death is significantly reduced. More importantly, we observed a significant difference in brain function, with the protected mice demonstrating significantly superior memory in lab tests," Dr Jiang said.
"This study has pinpointed a very promising drug target. We are now screening a large chemical library to find ways of effectively inhibiting this channel. Our ongoing research using animal models is testing whether blockage of this channel can offer protection again brain damage and cognitive dysfunction in stroke patients," Dr Jiang said.