Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 29,294 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
Wednesday, August 15, 2018
Paralyzed mice regain movement in their legs with new treatment
The drug reactivates nerve pathways in partially severed spinal cords.
Most
people with spinal cord injuries are paralyzed below the injury site,
even if the cord is only partially severed. Researchers don’t know why
the nerve pathways that are still intact also stop working. A new study provides a promising answer, and a path to restoring movement.
Researchers treated mice with partially severed spinal cords with a
compound called CLP209. The drug was administered over eight to ten
weeks. About 80 percent of the injured mice regained their ability to
take steps. “Stepping is a first step towards motor functional recovery
in animals, and perhaps humans,” says Boston Children’s Hospital
researcher Zhigang He, who led the study.
A new approach is paying off
Many animal studies attempting to repair spinal cord damage have focused
on getting nerve fibers to regenerate, or new ones to grow out of
remaining healthy fibers. He and other researchers have achieved this,
but they didn’t see the corresponding improvements in motor function
they had hoped for.
He and his coauthors decided to try a different approach. They were
inspired by treatments that stimulate the space around injured patients’
spinal cord with electric currents. When combined with rehabilitation
training, this stimulation is the only treatment for spinal cord injury
patients known to be effective. "However, in these studies, when you
turn off the stimulation, the effect is gone,” says He.
The researchers set out to see if they could use drugs to mimic the
stimulation caused by electric currents, so the effect would be
longer-lasting. They tested several compounds known to alter the
excitability of neurons. A small molecule called CLP209 worked best, and
the treated mice remained more mobile than untreated mice up to two
weeks after treatment stopped.
Results explain why remaining nerve pathways don’t function normally
The fact that CLP209 worked so well gives researchers a major clue as to
why even intact nerve pathways fail after a spinal cord injury. The key
seems to be a protein called KCC2, which CLP290 is known to activate.
To facilitate movement like walking, the spinal cord transmits the
brain’s commands to muscles with two types of signals: those that
inhibit muscles’ neurons and those that activate them. These opposing
signals are what allow muscles to work in pairs, with one relaxing while
the other contracts.
After a spinal cord injury, neurons that send signals inhibiting
movement don’t produce enough of the KCC2 protein. As a result of this
deficit, they don’t receive instructions from the brain to stop firing,
and the overall spinal circuit is overwhelmed with inhibitory signals.
When the mice were treated with CLP290, the drug restored KCC2 levels,
the brain’s commands to stop firing got through to inhibitory neurons,
and signals resulting in movement were no longer overpowered.
"Too much excitation is not good, and too much inhibition is not good
either,” says He. “You really need to get a balance. This hasn't been
demonstrated in a rigorous way in spinal cord injury before."
A cross section of a mouse spinal cord, stained two different ways,
showing increased expression of KCC2 in inhibitory neurons. Credit:
Zhigang He Lab, Boston Children's Hospital
More research is needed to determine the treatment’s full potential
He and his colleagues are now exploring other drugs to activate KCC2 in
spinal cord injuries. They hope their therapy could one day be combined
with electrical stimulation techniques to maximize patients’ recovery.
They also hope they won’t be alone in exploring this type of drug’s
potential. He says: “It would be great if other groups are willing to
try this in their injury models. We hope that collectively we could find
out the strengths and weaknesses of this approach and consider which
patient populations could be targeted.”
No comments:
Post a Comment