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SlagPosten's Innholdsoversikt / Table of contents |
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| 16.feb.1999
Hvorfor reparerer ikke kroppen selv hjerneskader? Og hva kan gjøres med det?
Why doesn't the body repair injuries to the brain? And what can be done about it?Weizmann Institute ANAHEIM, CA, January 24, 1999 -- New concepts, revealing a unique and surprising relationship between the central nervous and the immune systems, were presented today by Prof. Michal Schwartz of Israel's Weizmann Institute of Science at the annual meeting of the American Association for the Advancement of Science. Prof. Schwartz' findings, which have the potential for being further developed into clinical therapy, have also been published in the January 1999 issue of Nature Medicine: - In her latest study, documented in the January 1999 Nature Medicine
article, Prof. Schwartz and her team, in collaboration with a research
group headed by Prof. Irun Cohen of the Weizmann Insitute's Immunology
Department discovered that the same cells that cause autoimmune diseases
such as multiple sclerosis-- a condition in which the
immune system attacks the body's own tissues--can actually be useful in repairing
damage to the central nervous system!
Prof.
Michal Schwartz pluss/plus Mer/More: Scientists report a major advance in spinal cord repair By Nature Medicine, Researchers at the Weizmann Institute of Science, Israel, have successfully regenerated spinal nervs in rat that had undergone complete severing of the spinal cord. This adds to the hope that a clinical therapy to improve neurological function in patients with spinal cord injury could be developed. Michal Schwartz and colleagues used a novel technique that involves applying macrophages-white blood cells necessary for the successful healing of damaged tissue-to the transected nerves. Prior to injection into the lesion site of the spinal cord, the macrophages were exposed to segments of rat peripheral nerve ex vivo. Treated animals showed a significant recovery of limb movement. Furthermore, electrical stimulation on the spinal cord caused movement in several muscles of the hind limb ans histological analysis revealed that the severed cord was re-connected after the procedure. The researchers suggest that this method of injecting autologous macrophages into the site of spinal cord injury may have clinical potential in treating paraplegia.
7. feb. 1999 Nytt websted:
En Ny behandling for Afasi?A NEW APPROACH TO SPEECH RECOVERY
1. feb. 1999 THE MIAMI PROJECT TO CURE PARALYSISEtter masse leting (etter hva jeg trodde het "The Florida Project") har jeg endelig funnet linken overfor! Cell Lines Hold Surprising Potential for Replacing Lost Nerve Cells
Trond
26. jan. 1999 The Stroke Patient Support Pages (SPSP)Fra Nancy Lattimer på den amerikanske STROKE-L listen, har jeg mottatt en link til dette interessante Slag-webstedet (opprettet og drevet av pårørende til slagrammede.): The Stroke Patient Support Pages På disse sidene finnes det også oppdatert informasjon om Nevron-celle transplantasjons-forsøkene ved University of Pittsburgh Medical Center (UPMC) (se Transplantasjon av hjerneceller nedenfor på denne siden for flere detaljer, endel av disse detaljene er også med på The Stroke Patient Support Pages' oppdatering NB! Nytt! Når dere først besøker denne site'n så følg også linken: Doctors Ready To Harvest Cells for Brain Repair til flg. artikkel: HUMAN BRAIN TRANSPLANTATION PROTOCOL APPROVED TO REVERSE NERVE AND BRAIN DAMAGE. på: http://www.newswise.com/articles/CELLHRV.CED.html
NORA Neuro-Optometric Rehabilitation/habilitation Fra vår amerikanske bidragsyter og samarbeidspartner Rob Evan Hughes har jeg mottatt ovenstående link til en organisasjonen NORA, som spesialiserer seg på spørsmål om rehabilitering av skader på syns-evnen etter hjerneskader og slag. Her er eksempler på noen av temaene de behandler på sin webside: From our American contributor and partner, Rob Evan Hughes, I received this link (above) to an organization called NORA, which focuses on questions concerning the rehabilitation of damages to the visual system, following traumatic brain injuries and strokes. Below are some examples of the topics to be found at the NORA web site:
NORA er et veldig godt eksempel på den type website for slagrehabilitering, som Rob og jeg en tid har arbeidet for å få etablert i sporadisk samarbeide med tysk og amerikansk fagekspertise innen nevrologi (kfr. RNN-initiativet) Dessverre ser fremdriften i dette prosjektet foreløpig til å ha stoppet litt opp. NORA is a very good example of the kind of website dedicated to stroke and traumatic brain injury rehabilitation, that Rob and I have worked for some time to establish, sporadically in cooperation with German and American medical experts in the neurosciences.(cfr. the RNN initiative) Regrettably there has been little progress on this project lately.
Fra: Paraplegikerkredsen (Danmark) DR. CHARLES KHOURI'S
POSSIBLE BREAKTHROUGH IN
Rehabilitering
av Hjernestammeslag hos forsøksdyr
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14. feb. 1999
Norsk Svar Legedialog på Internett
10.feb.1999 John M. Heidemann, Jr. på STROKE-L la idag ut tips om flg. på listen.: Slangegift
i akuttbehandling av Slag
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| Neurophilin ligands are small molecules that have the potential to promote neurite outgrowth and accelerate recovery following nerve injury. They may play a future role in the treatment of a variety of acute and chronic neurological conditions. Neurophilin compounds designed by Vertex are orally deliverable, and have been shown to accelerate functional recovery and promote nerve growth in several different animal models of central and peripheral nervous system injury |
Timcodar (VX-853) for Peripheral Neuropathy
---------------------------------------
Cambridge, MA, November 10, 1998
NB: Jeg er IKKE aksjonær i Vertex! Men det ser jo ut som om de driver med forskning av stor interesse for oss.! Ikke sant?
NOTE: I'm not a Vertex stockholder! But it seems
they're into several research projects of great interest to us, doesn't
it? :-)
Trond
30. jan. 1999
http://www.med.usf.edu/PUBAFF/hot/sertoli.html
TESTICLE CELLS BOOST FUNCTION OF RAT BRAINS DAMAGED BY PARKINSON'S
Cells from the testes may one day enable neurosurgeons to improve the function of tissue damaged by Parkinson's disease, stroke or other neurodegenerative disorders, said the lead researcher for a University of South Florida study published today.
USF researchers found that rats with symptoms of Parkinson's improved significantly when Sertoli cells from rat testes were implanted into the brains of the rats. Furthermore, embryonic rat neurons added to Sertoli cell factors survived longer and grew more new fibers than neurons added to cultures without traces of Sertoli cells.
The study appears in the October issue of the journal Nature Medicine.
"The results suggest that Sertoli cells may help regrow the neural connections to the brain lost in Parkinson's or keep the remaining dopamine-producing brain cells alive," said Paul Sanberg, PhD, professor and director of neurosurgical research at USF.
Parkinson's disease gradually kills the cells that produce dopamine, a neurotransmitter needed for control of movement.
This latest Sertoli cell research builds upon a USF study published last year in Nature Biotechnology. That earlier study demonstrated that rat Sertoli cells successfully protected themselves and nearby transplanted cells from attack by the rat's own immune system. Normally the immune response in the rat's brain would have rejected the transplanted cells that were taken from another species.
But, Dr. Sanberg said, Sertoli cells release growth factors and other substances that appear to promote the survival and growth of transplanted grafts as well as ward off the brain's immune enforcer cells, called microglia.
The studies are a first step in exploring the clinical potential of Sertoli cells, said Thomas Freeman, M.D., USF associate professor of surgery.
If animal Sertoli cells suitable for human transplants could be found, Dr. Freeman said, they might be useful in increasing the survival of human neural transplants. Currently, fewer than 5 percent of the cells transplanted in the brain to restore normal dopamine levels survive in Parkinson's patients.
Another possibility is that Sertoli cells alone might actually be an alternative to neural tissue transplantation if they could be implanted in the brain early enough to arrest the progression of Parkinson's, Dr. Freeman said.
Other USF researchers for the Nature Medicine study were Drs. Cesario Borlongan, Agneta Othberg, Samuel Saporta, and Don Cameron.
Neurotrophic Factors :
ELEVATION OF BRAIN NEUROTROPHIN mRNA BY ORAL TREATMENT WITH AIT-082
1998 SOCIETY FOR NEUROSCIENCE Meeting in Los Angeles
AIT-082 is a novel small molecule that, in animals, crosses the blood-brain barrier to regenerate nerve function by increasing levels of neurotrophic growth factors and causing nerve sprouting in the brain. Pre-clinical studies in animals have demonstrated that AIT-082 improves memory in aged animals and in animals with neurological deficits.
Abstract:
The object of this study was to
determine whether AIT-082, a analog of hypoxanthine, modified the levels
of neurotrophins in the brains of mice with natural
age-induced memory deficits or rats with brain lesions. Previous studies
have shown that AIT-082 increased the levels of mRNA for NGF, NT-3 and
bFGF but not BDNF in cultures of astrocytes. Thirteen month old C57BL/6
mice received AIT-082 in their drinking water (equiv. to 30 mg/kg/day)
for ten months. A control group received no drug in their drinking
water.
During this period, mice were tested for working memory performance in
the win-shift paradigm, a delayed alternation positive reinforcement
task which measures the duration of the memory trace. At 23 months of
age, there was a clear difference between controls (no memory) and
AIT-082 treated (in which 50% of the mice exhibited no deficit). Mice
were sacrificed and brain tissue analyzed for neurotrophin mRNA using
RT-PCR technology. There was a significant increase in the mRNA for NGF,
NT-3 and bFGF in the frontal cortex and hippocampus but not the
cerebellum of animals that had functionally intact memory when compared
to animals that could not perform the memory task.
Bilateral lesions of the nucleus basalis of Meynert in 250 g male Wistar
rats produced by ibotenic acid lead to memory deficits when tested in
the Morris water maze. Treatment with AIT-082 (20 mg/kg/day in the
drinking water) ameliorated the memory impairment by 20 days after
lesion. The levels of neurotrophins were measured in lesioned animals
after treatment.
AIT-082 is orally active, rapidly penetrates the
blood brain barrier and induces the production of
multiple growth factors at the appropriate target sites in the
central nervous system.
AIT-082, a unique purine derivative, enhances nerve growth factor mediated neurite outgrowth from PC12 cells.
Middlemiss PJ, Glasky AJ, Rathbone MP, Werstuik E, Hindley S, Gysbers J
Department of Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada. middlems@fhs.csu.mcmaster.ca
AIT-082 is a novel, metabolically stable, derivative of the purine hypoxanthine. Addition of AIT-082 to cultured PC12 cells enhanced significantly nerve growth factor (NGF)-mediated neurite outgrowth from PC12 cells. These results suggest a cellular mechanism, the enhancement of NGF-action, that might account for the ability of AIT-082 to restore age-induced working memory deficits in mice.
PMID: 8584241, UI: 96156470
