This is seriously
fundamental and suggests that regeneration can be achieved and that it may even
turn out to be easy. That would be a serious
blessing for human health care if once and for all the human body can be
generally repaired. Removal of diseased
tissue will then be merely the prelude to outright replacement.
I think that we
can be very bullish with this. The path
is now spelled out as clearly as possible.
We have the on off switch in hand.
This will be an
enormous blessing and should also lead directly to protocols capable of reversing
brain damage as well. Imagine one system for removing the effects
of Alzheimer’s and a second to restore connectivity.
Scientists
identify clue to regrowing nerve cells
November 7, 2013
By Michael C. Purdy
To study how nerve cells respond to injuries in
their branches, Washington University researcher Valeria Cavalli grows them in
“spots” like the one shown above. Cavalli
recently identified a chain reaction that enables repair of these branches when
they are cut.
Researchers at Washington University School of Medicine in St. Louis
have identified a chain reaction that triggers the regrowth of some damaged
nerve cell branches, a discovery that one day may help improve treatments for
nerve injuries that can cause loss of sensation or paralysis.
The scientists also showed that nerve cells in the
brain and spinal cord are missing a link in this chain reaction. The link, a
protein called HDAC5, may help explain why these cells are unlikely to regrow
lost branches on their own. The new research suggests that activating HDAC5
in the central nervous system may turn on regeneration of nerve cell branches
in this region, where injuries often cause lasting paralysis.
“We knew several genes that contribute to the regrowth
of these nerve cell branches, which are called axons, but until now we didn’t
know what activated the expression of these genes and, hence, the repair
process,” said senior author Valeria Cavalli, PhD, assistant professor of
neurobiology. “This puts us a step closer to one day being able to develop
treatments that enhance axon regrowth.”
The research appears Nov. 7 in the journal Cell.
Axons are the branches of nerve cells that send
messages. They typically are much longer and more vulnerable to injury than
dendrites, the branches that receive messages.
In the peripheral nervous system — the network of
nerve cells outside the brain and spinal column — cells sometimes naturally
regenerate damaged axons. But in the central nervous system, comprised of the
brain and spinal cord, injured nerve cells typically do not replace lost
axons.
Working with peripheral nervous system cells grown
in the laboratory, Yongcheol Cho, PhD, a postdoctoral research associate in
Cavalli’s laboratory, severed the cells’ axons. He and his colleagues learned
that this causes a surge of calcium to travel backward along the axon to the
body of the cell. The surge is the first step in a series of reactions that
activate axon repair mechanisms.
In peripheral nerve cells, one of the most important
steps in this chain reaction is the release of a protein, HDAC5, from the
cell nucleus, the central compartment where DNA is kept. The researchers
learned that after leaving the nucleus, HDAC5 turns on a number of genes
involved in the regrowth process. HDAC5 also travels to the site of the injury
to assist in the creation of microtubules, rigid tubes that act as support
structures for the cell and help establish the structure of the replacement
axon.[
this sounds awfully fundamental to this observer – arclein ]
When the researchers genetically modified the HDAC5 gene
to keep its protein trapped in the nuclei of peripheral nerve cells, axons did
not regenerate in cell cultures. The scientists also showed they could
encourage axon regrowth in cell cultures and in animals by dosing the cells
with drugs that made it easier for HDAC5 to leave the nucleus.
When the scientists looked for the same chain
reaction in central nervous system cells, they found that HDAC5 never left the
nuclei of the cells and did not travel to the site of the injury. They believe
that failure to get this essential player out of the nucleus may be one of the
most important reasons why central nervous system cells do not regenerate
axons.
“This gives us the hope that if we can find ways to
manipulate this system in brain and spinal cord neurons, we can help the cells
of the central nervous system regrow lost branches,” Cavalli said. “We’re
working on that now.”
Cavalli also is collaborating with Susan Mackinnon, MD, the Sydney M. Shoenberg Jr. and Robert
H. Shoenberg Professor of Surgery, chief of the Division of Plastic and
Reconstructive Surgery and a pioneer in peripheral nerve transplants. The two
are investigating whether HDAC5 or other components of the chain reaction can
be used to help restore sensory functions in nerve grafts.
Funding from the National Institutes of Health
(DE022000 and NS082446), the McDonnell Center for Cellular and Molecular
Neurobiology, the Hope Center for Neurological Disorders and the National
Research Foundation of Korea supported this research.
Cho Y, Sloutsky R, Naegle KM, Cavalli V.
Injury-induced HDAC5 nuclear export is essential for axon regeneration. Cell,
online Nov. 7, 2013.
Washington
University School of Medicine’s 2,100 employed and volunteer faculty
physicians also are the medical staff of Barnes-Jewish andSt. Louis Children’s hospitals.
The School of Medicine is one of the leading medical research, teaching and
patient care institutions in the nation, currently ranked sixth in the nation
by U.S. News & World Report. Through its affiliations with
Barnes-Jewish and St. Louis Children’s hospitals, the School of Medicine is
linked to BJC
HealthCare.
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