Guest guest Posted November 10, 2004 Report Share Posted November 10, 2004 Study examines chemicals that regenerate nerves cellsBy MerrickApril 12, 2002http://www.jhunewsletter.com/vnews/display.v/ART/2002/04/12/3cb5c413be92cHopkins'>http://www.jhunewsletter.com/vnews/display.v/ART/2002/04/12/3cb5c413be92cHopkins scientists were able to successfully initiate nerve regenerationin rats researchers reported Monday at the 223rd national meeting of theAmerican Chemical Society.Dr. Schnaar, professor of pharmacology and neuroscience at sHopkins University Medical School, lead the study which may help providethe knowledge base for discoveries in human never regeneration to treatspinal cord injuries and diseases such as multiple sclerosis andParkinson's."In this study we have found one of the key players in the process bywhich nerves get the signal not to regenerate," said Schnaar, "byknowing that, we and others in the field can work together to developtechnologies to enhance nerve regeneration."Schnaar and collogues have found and identified four chemicals thatcaused damaged nerves to being regenerating. The experiments wereconducted on cells in a petri dish, and thus this research has a longway to go before it could have any practical application to treatingnerve diseases in humans.Normal, healthy nerve cells are wrapped in an outer cellular sheetcalled myelin. Myelin acts like the insulation surrounding an electricalwire, and helps strengthen the electrical signal. Diseases such asmultiple sclerosis are caused by a degeneration of the myelin sheet andthus a loss in nerve signal conductance."Myelin also has a dark side," Schnaar said. "When nerve axons aredamaged, such as in spinal cord injuries, myelin stops them fromregenerating. In large part, myelin blockade of axon regeneration isresponsible for the lack of recovery from a nervous system injury."During normal growth and development myelin cells make specific contactswith their axons and exchange molecular signals. Nerve cell injuryhowever, disrupts these normal signaling pathways and causes the myelinto block the nerve cell from regenerating.Despite the very promising results of his experiments, Schnaarcautioned, "nerve damage is very much more complex than our laboratoryconditions and this new knowledge, by itself, is unlikely to provide aidto those suffering with nerve injury. However, it is our hope that ourdiscoveries, along with other new discoveries on the molecular basis fornerve regeneration, will help in the search for therapies to improvefunctional recovery after nervous system injury or disease."Rashmi Bansal, professor of neuroscience at the University ofConnecticut Medical School in Farmington, told United PressInternational commented that Schnaar's research "is at the forefront ofa current recognition of the fundamental importance of this class oflipids in biomedical science.""There are important implications here for pathological situations, inparticular nerve regeneration after injury or degenerative diseases,including multiple sclerosis, a disease in which nerve deterioration hasrecently been re-emphasized," Bansal added.Schnaar is continuing his work to see if he can reproduce his findingsin a living system, but he does not have preliminary results quite yet."We are getting at the mechanisms that underlie one of the problems innerve regrowth but there are others," Schnaar said. "There is no magicformula for spinal cord repair."Schnaar emphasized some of the difficulties in applying this knowledgeabout rat nerve cells to human cells."In the human body, nerve damage is much more complicated than it is inour laboratory conditions, and this new knowledge, by itself, isunlikely to solve the problem of nerve regeneration," says Schnaar."However, it is our hope that our discoveries, along with other newdiscoveries on the molecular basis for nerve regeneration, will help inthe search for therapies to improve functional recovery after nervoussystem injury or disease."http://www.jhunewsletter.com/vnews/display.v/ART/2002/04/12/3cb5c413be92c Quote Link to comment Share on other sites More sharing options...
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