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.
Stroke
Stroke can cause permanent disability and it is important to recognize its early warning signs to stop its progress. Early warning signs of stroke include sudden weakness of facial muscles.
Advertisement
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.
Co-author Dr Lin-Hua Jiang, of the University of Leeds' School of Biomedical Sciences, said: "Until now, much of the drug research has been focussing 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 underway after patients have been admitted to hospital."
![How to Deal with a Stroke]( "How to Deal with a Stroke")
Stroke is a brain attack, which occurs when the blood supply to the brain is interrupted. It affects all age groups; according to the WHO, 15 million people are affected by stroke annually.
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.
Source: Eurekalert
How to Deal with a Stroke
Stroke is a brain attack, which occurs when the blood supply to the brain is interrupted. It affects all age groups; according to the WHO, 15 million people are affected by stroke annually.
Advertisement
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.
Source: Eurekalert
Stress and the Gender Divide
Stress has become entwined in the current lifestyle of a young working couple and has resulted in the rise in incidence of hypertension, diabetes and psychosomatic illnesses.
Advertisement
Advertisement
|
Advertisement
Recommended Reading
Latest Research News
A recent clinical trial suggests that the first medication therapy to reduce the progression of nearsightedness in children could be on the way.
Autoimmune disorders were found to be linked to Sjogren's, systemic lupus erythematosus, and systemic sclerosis.
Successful brain pacemaker implantation has helped a 51year old Parkinson's disease patient to revitalize her quality of life.
Recent recommendations on lifestyle behaviors to prevent progression of rheumatic and musculoskeletal diseases revealed.
The study offers insights into how psoriasis can trigger diabetes, heart disease, and inflammatory bowel disease.