Researchers have pinpointed a mechanism linked to the brain damage often sustained by stroke survivors, according to a news release from the University of Leeds. The release reports that a team from the University of Leeds and Zhejiang University in China studied the second phase of stroke, known as “oxidative stress,” which occurs in the hours and days after blood supply resumes.
The researchers report that they discovered a mechanism in neurons that, if removed, helped reduce the damage to brain function.
Lin-Hua Jiang, BSc, MSC, PhD, study co-author, University of Leeds’ School of Biomedical Sciences, points out in the release that, “Until now, much of the drug research has been focusing on the direct damage caused by the loss of blood flow, but this phase can be hard to target. The patient may not even be in the ambulance when it is happening. We have found a mechanism that is linked to the next phase of damage that will often be under way after patients have been admitted to hospital.”
The release notes that the study was designed to investigate 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 rises post-stroke to levels that are harmful to neurons, the release says.
Jiang adds that the researchers 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,” Jiang says.
During the study, researchers compared the impact of strokes on mice with TRMP2 with a transgenic strain without it. Jiang explains that in mice in which the TRMP2 channel does not function, the reactive oxygen species are still produced but the neurons are protected. The neuronal death is also reportedly significantly reduced, and the researchers observed a significant difference in brain function, with the protected mice demonstrating significantly superior memory in lab tests.
Thanks to the study’s findings, Jiang reports that a promising drug target has been discovered, and “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.”
[Source(s): ScienceDaily, University of Leeds]