Would this help stroke survivors? We'll never know because we have NO stroke leadership or strategy to followup promising research. You're screwed once again.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=168700&CultureCode=en
Releasing molecular brake allowed damaged neurons to regenerate
Injuries
to the spinal cord can cause paralysis and other permanent disabilities
because severed nerve fibers do not regrow. Now, scientists of the
German Center for Neurodegenerative Diseases (DZNE) have succeeded in
releasing a molecular brake that prevents the regeneration of nerve
connections. Treatment of mice with “Pregabalin”, a drug that acts upon
the growth inhibiting mechanism, caused damaged nerve connections to
regenerate. Researchers led by neurobiologist Frank Bradke report on
these findings in the journal “Neuron”.
Human nerve cells are interconnected in a network that extends to all
parts of the body. In this way control signals are transmitted from
head to toe, while sensory inputs flow in the opposite direction. For
this to happen, impulses are passed from neuron to neuron, not unlike a
relay race. Damages to this wiring system can have drastic consequences –
particularly if they affect the brain or the spinal cord. This is
because the cells of the central nervous system are connected by long
projections. When severed, these projections, which are called “axons”,
are unable to regrow.
Reawakening a lost talent
Neural pathways that have been injured can only regenerate if new
connections arise between the affected cells. In a sense, the neurons
have to stretch out their arms, i.e. the axons have to grow. In fact,
this happens in the early stages of embryonic development. However, this
ability disappears in the adult. Can it be reactivated? This was the
question Professor Bradke and co-workers asked themselves. “We started
from the hypothesis that neurons actively down-regulate their growth
program once they have reached other cells, so that they don’t overshoot
the mark. This means, there should be a braking mechanism that is
triggered as soon as a neuron connects to others,” says Dr. Andrea
Tedeschi, a member of the Bradke Lab and first author of the current
publication.
Searching through the genome
In mice and cell cultures, the scientists started an extensive search
for genes that regulate the growth of neurons. “That was like looking
for the proverbial needle in the haystack. There are hundreds of active
genes in every nerve cell, depending on its stage of development. To
analyze the large data set we heavily relied on bioinformatics. To this
end, we cooperated closely with colleagues at the University of Bonn,”
says Bradke. “Ultimately, we were able to identify a promising
candidate. This gene, known as Cacna2d2, plays an important role in
synapse formation and function, in other words in bridging the final gap
between nerve cells.” During further experiments, the researchers
modified the gene’s activity, e.g. by deactivating it. In this way, they
were able to prove that Cacna2d2 does actually influence axonal growth
and the regeneration of nerve fibers.
Pregabalin triggered neuronal growth
Cacna2d2 encodes the blueprint of a protein that is part of a larger
molecular complex. The protein anchors ion channels in the cell membrane
that regulate the flow of calcium particles into the cell. Calcium
levels affect cellular processes such as the release of
neurotransmitters. These ion channels are therefore essential for the
communication between neurons.
In further investigations, the researchers used Pregabalin (PGB), a
drug that had long been known to bind to the molecular anchors of
calcium channels. Over a period of several weeks, they administered PGB
to mice with spinal cord injuries. As it turned out, this treatment
caused new nerve connections to grow.
“Our study shows that synapse formation acts as a powerful switch
that restrains axonal growth. A clinically-relevant drug can manipulate
this effect,” says Bradke. In fact, PGB is already being used to treat
lesions of the spinal cord, albeit it is applied as a pain killer and
relatively late after the injury has occurred. “PGB might have a
regenerative effect in patients, if it is given soon enough. In the long
term this could lead to a new treatment approach. However, we don’t
know yet.”
A new mechanism?
In previous studies, the DZNE researchers showed that certain cancer
drugs can also cause damaged nerve connections to regrow. The main
protagonists in this process are the “microtubules”, long protein
complexes that stabilize the cell body. When the microtubules grow,
axons do as well. Is there a connection between the different findings?
“We don’t know whether these mechanisms are independent or whether they
are somehow related,” says Bradke. “This is something we want to examine
more closely in the future.”
https://www.dzne.de/en/about-us/public-relations/news/2016/press-release-no-16
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