So human clinical testing needed. What is your doctor and hospital doing to facilitate that? ANYTHING AT ALL? Are your doctor and hospital responsible for anything in stroke? Maybe burying their heads in the sand so they don't have to tackle any of the BHAGs(Big Hairy Audacious Goals) of 100% recovery for all survivors.
Was any followup done from Sept. 2017 when this came out? NO? then get your stroke hospital president and board of directors fired for incompetence.
Ginsenoside Rg1 provides neuroprotection against blood brain barrier disruption and neurological injury in a rat model of cerebral ischemia/reperfusion through downregulation of aquaporin 4 expression Sept. 2017
Novel stroke therapy reduces brain damage in mice: Study
Press Trust of India |
Tokyo
Last Updated at May 14, 2019 16:36 IST
An experimental treatment for stroke can help restore
movement and reduce brain cell damage in mice, a study has found, paving
the way for new therapies to help victims of debilitating brain
injuries recover.
Stroke -- a condition in which poor blood flow to the brain results in cell death -- requires time-sensitive treatment, researchers said.
Clotting factors like thrombin are commonly administered to patients, but there are many other stroke-related signs that can be targeted, such as swelling and ion imbalances in the surrounding fluids.
The study, published in the journal Proceedings of the National Academy of Sciences, shows that brain fluids can be normalised with adrenergic receptor antagonists -- a combination of drugs to block the activity of adrenaline in the brain.
The experimental treatment for stroke aided motor recovery and reduced cell death in mice, scientists said.
A major consequence of stroke is an immediate imbalance in the ion concentrations of fluids that bathe brain cells. Potassium levels spike and fluid accumulates, which leads to swelling, a major cause of stroke injury.
"We know that the water dynamics in the brain immediately during and after a stroke are critical, so we focused on the pathways that move fluids in and out of cells," said Hiromu Monai of the RIKEN Center for Brain Science and Ochanomizu University in Japan.
One way to lower potassium and get neurons active again is by administering adrenergic receptor (AdR) antagonists, drugs that counteract the electrical and chemical disturbance that accompanies a stroke.
These antagonist drugs have been found to promote fluid exchange in normal brains, according to Maiken Nedergaard of the University of Rochester Medical Center in the US.
A cocktail of AdR blockers was successful in reducing both the area of tissue damage and potassium levels in stroked mice.
Moreover, even one or two hours post-stroke, administration of AdR blockers was effective in stopping the infarct from spreading. Mice were also able to recover the use of their forepaw much more quickly when treated with AdR blockers.
The researchers found that levels of a water channel called aquaporin 4 were lower following a stroke.
"We think that preserving aquaporin levels is critical to protecting brain tissue during stroke," said Monai.
To test this idea, they used genetically engineered mice that lacked the aquaporin 4 water channel.
These mice did not benefit from AdR blocker treatment and their brain potassium levels remained high after stroke, supporting the idea that the neuroprotective effect occurs through the action of aquaporin 4 water channels.
"Keeping potassium levels in balance is an alternative therapeutic strategy for stroke, and we found that adrenergic receptor blockers promote this normalization," said Monai.
"Recovering motor function following a stroke is so important, and we also saw improvements in the mice treated with AdR blockers," he said.
Stroke -- a condition in which poor blood flow to the brain results in cell death -- requires time-sensitive treatment, researchers said.
Clotting factors like thrombin are commonly administered to patients, but there are many other stroke-related signs that can be targeted, such as swelling and ion imbalances in the surrounding fluids.
The study, published in the journal Proceedings of the National Academy of Sciences, shows that brain fluids can be normalised with adrenergic receptor antagonists -- a combination of drugs to block the activity of adrenaline in the brain.
The experimental treatment for stroke aided motor recovery and reduced cell death in mice, scientists said.
A major consequence of stroke is an immediate imbalance in the ion concentrations of fluids that bathe brain cells. Potassium levels spike and fluid accumulates, which leads to swelling, a major cause of stroke injury.
"We know that the water dynamics in the brain immediately during and after a stroke are critical, so we focused on the pathways that move fluids in and out of cells," said Hiromu Monai of the RIKEN Center for Brain Science and Ochanomizu University in Japan.
One way to lower potassium and get neurons active again is by administering adrenergic receptor (AdR) antagonists, drugs that counteract the electrical and chemical disturbance that accompanies a stroke.
These antagonist drugs have been found to promote fluid exchange in normal brains, according to Maiken Nedergaard of the University of Rochester Medical Center in the US.
A cocktail of AdR blockers was successful in reducing both the area of tissue damage and potassium levels in stroked mice.
Moreover, even one or two hours post-stroke, administration of AdR blockers was effective in stopping the infarct from spreading. Mice were also able to recover the use of their forepaw much more quickly when treated with AdR blockers.
The researchers found that levels of a water channel called aquaporin 4 were lower following a stroke.
"We think that preserving aquaporin levels is critical to protecting brain tissue during stroke," said Monai.
To test this idea, they used genetically engineered mice that lacked the aquaporin 4 water channel.
These mice did not benefit from AdR blocker treatment and their brain potassium levels remained high after stroke, supporting the idea that the neuroprotective effect occurs through the action of aquaporin 4 water channels.
"Keeping potassium levels in balance is an alternative therapeutic strategy for stroke, and we found that adrenergic receptor blockers promote this normalization," said Monai.
"Recovering motor function following a stroke is so important, and we also saw improvements in the mice treated with AdR blockers," he said.
(This story has not been edited by Business Standard staff and is auto-generated from a syndicated feed.)
