This is a good introduction to
the internal behavior of brain tissue under impact stress. It is highly appropriate as we are now
entering an age in which in which brain concussion in sports will no longer be
tolerated and this clearly shows us the intricacies of damage repair. More specifically, it makes sequential concussion
an extremely dangerous practice.
That the human brain is even able
to substantially recover is not good enough as we have seen from the recent
outcry coming out of Football and Hockey.
It will take a while, but concussion risk has to be almost eliminated in
all sports. Accidents can be accepted as
a part of any sport however dangerous it appears, although we are also
exploring limits there also.
The point is that the head cannot
be used as a weapon and the head cannot be targeted. Let us make it that simple. It may even make it possible to box while
doing all that. It has long been obvious
that there is no safe level of concussion that can be tolerated as a matter of
custom, so out with it!
Scientists learn how stem cell implants help heal traumatic brain
injury
Public release date: 12-Jan-2012
Contact: Jim Kelly
For years, researchers seeking new therapies for traumatic brain injury
have been tantalized by the results of animal experiments with stem cells. In
numerous studies, stem cell implantation has substantially improved brain
function in experimental animals with brain trauma. But just how these
improvements occur has remained a mystery.
Now, an important part of this puzzle has been pieced together by
researchers at the University of Texas Medical Branch at Galveston
A significant component of traumatic brain injury, traumatic axonal
injury involves damage to axons and dendrites, the filaments that extend out
from the bodies of the neurons. The damage continues after the initial
trauma, since the axons and dendrites respond to injury by withdrawing back to
the bodies of the neurons.
"Axons and dendrites are the basis of neuron-to-neuron
communication, and when they are lost, neuron function is lost," said UTMB
professor Ping Wu, lead author of a paper on the research appearing in the Journal
of Neurotrauma. "In this study, we found that our stem cell
transplantation both prevents further axonal injury and promotes axonal
regrowth, through a number of previously unknown molecular mechanisms."
The UTMB researchers began their investigation with a clue from their
previous work: they had determined that their neural stem cells secreted a
substance called glial derived neurotrophic factor, which seemed to help
injured rat brains recover from injury. As a first step toward identifying the
processes by which GDNF and neural stem cell transplantation produced their
beneficial effects, Wu enlisted UTMB professors Larry Denner, Douglas Dewitt
and Dr. Donald Prough to use proteomic techniques to compare injured rat brains
with injured rat brains into which neural stem cells had been transplanted.
"We identified about 400 proteins that respond differently after
injury and after grafting with neural stem cells," Wu said. "When we
grouped them using a state-of-the-art Internet database, we found that a group
of cytoskeleton proteins was being changed, and in particular one called
alpha-smooth muscle actin, which had never been reported in the neurons
before."
Because so many of the proteins that changed were related to axonal
structure and function, the UTMB scientists then focused on traumatic axonal
injury. Initially working with rats, they confirmed that axons and dendrites
suffered damage from trauma; implanted neural stem cells reduced this harm, as
well as lowering levels of alpha-smooth muscle actin inside neurons that were
raised after trauma.
To probe further into the molecular details of GDNF's role in reducing
traumatic axonal injury, the researchers used a system in which human neurons
were placed on a flexible membrane that was then suddenly distended with a
precisely calibrated puff of gas. Their goal was to simulate the sudden
compression and stretching forces exerted on brain cells by a blow to the head.
Initial results from this "rapid stretch injury model"
matched those seen in rat experiments, with GDNF protecting axons and dendrites
from additional damage in the period after trauma and significantly reducing
alpha-smooth muscle actin levels boosted by the simulated injury. In addition,
they found evidence linking alpha-smooth muscle actin with RhoA, a small
protein that blocks axonal growth after injury. Finally, again taking a cue
from their proteomic study, they turned their attention to one component of a
protein known as calcineurin, finding that it interacted with GDNF to protect
axons and dendrites in the RSI model.
"We're quite excited about these discoveries, because they're
highly novel — we now know much more about how GDNF protects axons and
dendrites from further injury and promotes their re-growth after trauma,"
Wu said. "This kind of detailed study is essential to developing safe and
effective therapies for traumatic brain injury."
###
Other authors of the Journal of Neurotrauma paper include
graduate students Enyin Wang, Junling Gao and Tiffany Dunn; assistant research
lab director Margaret Parsley; Qin Yang of Huazhong University of Science and
Technology in Wuhan, China, Lin Zhang of Sichuan University in Chengdu, China;
and professors Douglas DeWitt, Larry Denner and Donald Prough. Support for this
research was provided by the U.S. Army, the Coalition for Brain Injury
Research, the Moody Center for Traumatic Brain and Spinal Cord Injury Research,
Mission Connect, the TIRR Foundation, the China Scholarship Council, the John
S. Dunn Research Foundation and the Cullen Foundation.
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