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An interesting article.............
November 1, 2000-Boston, MA-Scientists at Children's Hospital Boston
have
described an important mechanism controlling axon regeneration in nerve
cells. Their discovery is reported in today's issue of The Journal of
Neuroscience. This work was sponsored in part by Boston Life Sciences,
Inc. (NASDAQ: BLSI) which is the exclusive commercial licensee of this
technology for all therapeutic indications including spinal cord injury,
stroke and glaucoma.
"This paper describes for the first time a central program that
controls a
whole family of genes required for axon growth, and that Inosine can
directly switch on this program," stated Dr. Larry Benowitz, senior
author
of the paper. "We previously published on the extraordinary
axon-regenerative properties of Inosine in vivo. These findings help
explain why Inosine has such dramatic positive effects after brain and
spinal cord injury."
Normally, central nervous system (CNS) cells are unable to re-grow damaged
fibers. Consequently, when such disruption occurs, their communication
with other nerve cells is lost, causing debilitating losses in function
for victims of stroke or traumatic injury. In a previously published paper
(PNAS, November 9, 1999), a group led by Dr. Larry Benowitz reported that
Inosine, a naturally occurring small molecule that is normally found in
low levels in the brain, can promote extensive axon sprouting in animals
with spinal cord injury. In the current paper, Dr. Larry Benowitz (senior
author) and co-workers describe the mechanism by which Inosine apparently
works. Benowitz and his group are hopeful that by activating neurons with
Inosine (as demonstrated in previous in vivo animal studies), they may be
able to achieve regenerative axon growth in humans whose central nervous
systems have sustained injury in stroke and spinal cord trauma.
The new findings indicate that Inosine passes right through the nerve
cell's membrane and activates an enzyme that appears to be the "master
switch" that controls the cell's molecular program for axon growth
(the
existence of this enzyme was first suggested by work from the laboratory
of Lloyd Greene at Columbia University). This same mechanism is believed
to be activated when brain cells are forming their connections during
embryonic development. In their studies, Dr. Benowitz and his group found
that this Inosine-activated program causes nerve cells to switch on a set
of genes that encode the proteins essential for nerve regeneration. In the
adult brain, this cellular program is normally silent, and nerve cells
that have been injured (e.g. by stroke) are not able to regenerate their
axons. Nevertheless, as described in this paper, this genetic program can
be reactivated by Inosine. Benowitz's group is close to isolating the
actual gene that encodes the enzyme upon which Inosine works. This, in
turn, will enable them to gain further valuable and clinically relevant
insights into the possibilities for regenerative axon growth in nerve
cells.
"We knew from previous studies that there is a whole set of genes
that are
commonly activated only when nerve cells are forming their connections.
However, we didn't know whether the expression of these genes was
controlled through separate pathways that are activated by different
growth factors, or whether there was a 'master switch', onto which
different signals converge to control the entire molecular program for
axon growth. Our findings indicate that the regenerative effects of growth
factors are mediated through this final common pathway," added Dr.
Benowitz.
Benowitz, whose work in this area was sponsored by Boston Life Sciences,
Inc. and the National Institutes of Health, is the Director of the
Laboratories for Neuroscience Research in Neurosurgery at Children's
Hospital and a member of the faculty of Harvard Medical School. Other
investigators involved in this study included Barbara Petrausch and
Claudia Stuermer from the University of Konstanz (Germany), Daniel Goldman
from the University of Michigan, and Raymond Tabibiazar, Timo Roser, Yun
Jing, and Nina Irwin, members of Benowitz's group at Children's Hospital.
"We are delighted with the publication of this breakthrough paper,
and
congratulate Dr. Benowitz and his team on this landmark discovery,"
stated
Dr. Marc Lanser, Chief Scientific Officer of BLSI. "Investigations
into
the mechanism by which Inosine stimulates such impressive axon
regeneration in animals have led directly to the discovery of this
important general principle regulating all of axon regeneration. We
believe that the addition of this 'master switch' to our licensed patent
portfolio reinforces BLSI's prominent position in the field of CNS
regeneration. We at BLSI plan to continue to advance the work of Dr.
Benowitz's team to its full scientific and commercial potential. We hope
to have Inosine in the clinic sometime next year for the treatment of
stroke and other CNS disorders," added Dr. Lanser.
Children's Hospital Boston is the nation's premier pediatric medical
center. Founded in 1869 as a 20-bed hospital for children, today it is a
300-bed comprehensive center for pediatric and adolescent health care
grounded in the values of excellence in patient care and sensitivity to
the complex needs and diversity of children and families. Children's
Hospital is the primary pediatric teaching affiliate of Harvard Medical
School, home to the world's leading pediatric research enterprise, and the
largest provider of health care to the children of Boston.
Thank you for taking the time to read this article.
EraseMS.com Team