A Canadian-led research team believes it has discovered a way to prevent the most devastating effects of stroke.
During a stroke, the brain is deprived of oxygen and nutrients, which strangles neurons, causing debilitating long-term impairment in motor function, memory and speech.
There are currently no drugs available to prevent the death of these cells and protect patients from their life-altering effects.
But a team of researchers, led by Dr. Michael Tymianski, a neurosurgeon at the Krembil Neuroscience Centre at Toronto Western Hospital, has found a method that protect neurons from this damage in rats, paving the way for new drugs that may keep cells alive even when blood stops flowing.
Previous studies in the field have focused mainly on finding new ways to restore blood to the brain as quickly as possible or on trying to block toxic chemicals that build up when cells experience stress, said Tony Hakim, director of the Canadian Stroke Network, which supported the study.
But the current research, reported Sunday in the journal Nature Neuroscience , takes a new approach, focusing on an ion channel named TRPM7 ("Trip-M7").
TRPM7 is found in cells throughout the body and the researchers had a hunch that the channels play a key role in cell death following oxygen deprivation.
To test their theory, Dr. Tymianski's team took healthy rats and injected a virus that suppressed the expression of TRPM7 directly into the hippocampus - the delicate brain region that is crucial for learning and memory.
They then cut off blood flow to the rats' brains for 15 minutes and compared the extent of damage days later to rats whose brains had not been treated before deprivation.
As expected, untreated rats with intact TRPM7 suffered severe neurological damage, with long-term impairment, including difficulty learning and remembering how to navigate a maze.
But the rats whose TRPM7 had been suppressed exhibited none of the expected damage. In fact, the treated rats performed just as well in memory tests as rats that had never been subjected to oxygen deprivation. And they exhibited no other side effects from the treatment.
"To the best of our knowledge, our results are the first to demonstrate that suppressing TRPM7 in adult mammals is feasible and that this markedly reduces delayed neuron death after ischemia," they write.
Because TRPM7 is found in virtually every tissue of the body, the team thinks they may have discovered the key to preventing cell death caused by reduced oxygen and nutrient supply, not just in neurons, but in other cells as well.
"It has tremendous implications," Dr. Tymianski said. "It is conceivable that the same types of processes occur in other tissues where there's ischemia as well."
This means the findings could apply to cell death seen in heart attacks, diabetes-related kidney and retinal problems, glaucoma, Parkinson's disease and Alzheimer's disease.
The next step, he said, will be to develop drugs that target TRPM7 channels that can eventually be administered to stroke patients to stave off the devastating effects of oxygen deprivation.
Dr. Tymianski said he hopes to have drugs ready for testing on animals in a year or two.
But University of Calgary neurologist and Heart & Stroke Foundation spokesman Michael Hill urged caution in interpreting the results. This is not the first time, he said, that receptors found to be crucial in cell death in the lab have failed to translate into viable therapies.
"Whether it can be translated to humans remains to be seen," he said.