IN-1 inhibitors

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 
FASEB Journal...

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
Newsgroups: sci.bio.evolution

[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
   DAMAGE

   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
   lifetime.

   "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
   injury."

   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
   priorities.
     _________________________________________________________________

danny
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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