A mechanism implicated in the brain damage experienced by stroke patients has been identified by researchers from the University of Leeds in the UK and Zhejiang University in China. The scientists are now looking for effective drug therapies to prevent this damage.

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As the blood supply resumes in the brain in the days following a stroke, “oxidative stress” can damage the memory and cognitive function of the patient.

When someone has a stroke, the blood supply to part of their brain is cut off. As the blood supply resumes in the brain in the days following the stroke, “oxidative stress” can damage the memory and cognitive function of the patient.

The researchers behind the new study say that, up until now, most of the research into potential drug therapies to treat stroke-related brain damage has focused on the initial damage caused by the loss of blood flow, rather than the damage from oxidative stress. However, this initial damage is hard to target.

“The patient may not even be in the ambulance when it is happening,” says co-author Dr. Lin-Hua Jiang, of the University of Leeds’ School of Biomedical Sciences. “We have found a mechanism that is linked to the next phase of damage that will often be underway after patients have been admitted to the hospital.”

Studying the oxidative stress phase of stroke-related brain damage in a mouse model, the team found a mechanism in neurons that – if removed – reduces the level of damage.

Dr. Jiang explains:

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.”

Investigating this ion channel further, the team compared the effects of stroke in mice with active TRPM2 and in those with inactivated TRPM2. They found that neurons were better protected from the oxidative stress in mice that had a disabled TRPM2 channel.

“The neuronal death is significantly reduced,” says Dr. Jiang. “More importantly, we observed a significant difference in brain function, with the protected mice demonstrating significantly superior memory in lab tests.”

The researchers believe they have pinpointed “a very promising drug target.” Next, they will screen a large database of chemicals to find a way of inhibiting the TRPM2 channel. The team will continue testing in animal models to see how effective blocking TRPM2 is for protecting against brain damage and cognitive dysfunction following a stroke.

In May, Medical News Today reported on a study from researchers at Ohio State University Wexner Medical Center, which suggested that a daily dose of vitamin E could prevent or reduce brain damage from stroke.

The Ohio State researchers were particularly interested in tocotrienol – a type of vitamin E found in palm oil that reduces cholesterol. They found that tocotrienol increased the diameter of arteries in response to oxygen demand – an effective means of preventing brain damage.