kenneth paul collins
KPCollins at postoffice.worldnet.att.net
Tue Oct 1 00:19:26 EST 1996
Melanie Popek wrote:
> I am writing a paper for a neuro course I am in and I am interested
> in writing about the new research being done with IN-1 antibodies
> for neural regrowth. If anyone knows of any articles that I may use,
> please let me know. I am having a difficult time finding information.
> Thanks in advance,
> Melanie Popek
see the 21 Sep 96 issue of _Science News_ p180, primary source Sep 96 issue of
also, here's something on it copied from sci.bio.evolution: (the experimental
results are new, the explanatory rationale is =old=)
Subject: brain evolution
Date: 23 Sep 1996 21:28:34 GMT
From: Danny Fagandini <daaf at cerium.demon.co.uk>
Organization: University of Washington
[moderator's note: Danny first sent me an AP wire release, which I
declined to post due to copyright concerns, but here's a "safe"
version of the same thing. Anyone want to comment? - JAH]
here is a version straight from the horse's mouth
with no copyright. I hope it still loooks interesting:
NEW CONCEPT EXPLAINS WHY MAMMALS CAN'T REPAIR CENTRAL NERVOUS SYSTEM
REHOVOT, ISRAEL -- September 17, 1996...Why is it that humans and
other mammals are left permanently paralyzed or otherwise handicapped
by injuries to the central nervous system, while fish and other
"lower" life forms can repair such injuries and resume normal lives?
A study led by Prof. Michal Schwartz of the Weizmann Institute of
Science, reported in the September issue of The FASEB Journal (the
official publication of the Federation of American Societies for
Experimental Biology), provides an explanation that links the
mammalian inability to repair central nerve damage with evolution --
and offers hope for developing an effective treatment for injuries to
the spinal cord and other parts of the central nervous system.
Evolution allowed mammals to have complex brains, capable of acquiring
new knowledge throughout a lifetime. But, according to Schwartz, along
with this asset came a disadvantage: the brain and the rest of the
central nervous system lost their self-healing ability, which exists
in lower vertebrates. Schwartz says this loss probably occurred as a
result of the critical need to protect the brain from remodeling by
the immune system: while immune cells normally help to heal damaged
tissue, their access to the brain would disrupt the complex and
dynamic neuronal networks that build up during an individual's
"There seems to have been an evolutionary trade-off," Schwartz says.
"Higher animals protected their central nervous system from invasion
by the immune system, but paid the price of forfeiting their ability
to regenerate injured nerves. Thus, an evolutionary advantage that
protects the healthy brain turns into a disadvantage in the case of
Generally, when tissue damage occurs, immune cells known as
macrophages swarm to the injured site, where they remove damaged cells
and release substances that promote healing. The central nervous
system in mammals is an exception in this regard: when damaged, it is
not effectively assisted by the immune system.
Schwartz's team found that this is because the mammalian central
nervous system contains an active component that suppresses the
macrophages. As a result, relatively few macrophages are recruited to
central nervous system injuries, and those that are recruited fail to
become "activated" and are ineffective.
"We have shown that the immune system's assistance is just as vital
for the repair of the mammalian central nervous system as it is for
any other tissue," Schwartz says. "However, because of a suppressive
mechanism which seems to have developed in the course of evolution,
this assistance does not operate."
The explanation emerged from a series of experiments conducted by a
Weizmann Institute Neurobiology Department team that included Orly
Lazarov-Spiegler, Adi Ben Zeev-Brann, David Hirschberg and Dr. Vered
Lavie, working with Dr. Arieh S. Solomon of the Sheba Medical Center
near Tel Aviv.
"Educating" immune cells
The scientists examined whether this obstacle to nerve regeneration
could be overcome by using macrophages that had been "educated" by
special treatment outside the body. For this purpose, rat macrophages
were first isolated and then activated through incubation with injured
sciatic nerves, which, as part of the peripheral nervous system, are
capable of regeneration. The scientists then transplanted the
activated macrophages into injured rat optic nerves, which, as part of
the central nervous system, normally do not regenerate.
The pre-activated macrophages induced the optic nerves to regrow.
"Macrophages may be the missing link in the process of wound-healing
in the central nervous system," Schwartz says. Transplanting suitably
activated macrophages into injured nerves may help overcome the
central nervous system,s failure to respond after injury. According to
Schwartz, the procedure might eventually be developed into a novel,
practical and potent treatment to repair central nervous system
injuries, and particularly to restore movement in cases of spinal
injury although such a development may still take many years. "This
approach would in effect mean turning the evolutionary clock back to
the distant past," Schwartz says.
Prof. Schwartz holds the Maurice and Ilse Katz Chair of
Neuroimmunology at the Weizmann Institute. The study was supported in
part by the Alan T. Brown Foundation of Nerve Paralysis, and by the
donation of Ralph Colton to the Weizmann Institute/University of
Michigan scientific exchange program.
The Weizmann Institute of Science, in Rehovot, Israel, is one of the
world's foremost centers of scientific research and graduate study.
Its 2,400 scientists, students, technicians, and engineers pursue
basic research in the quest for knowledge and the enhancement of the
human condition. New ways of fighting disease and hunger, protecting
the environment, and harnessing alternative sources of energy are high
daaf at cerium.demon.co.uk
People hate because they fear, and they fear because
they do not understand, and they do not understand
because hating is less work than understanding.
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