Published by the Students of Johns Hopkins since 1896
April 26, 2024

Study examines chemicals that regenerate nerves cells

By David Merrick | April 11, 2002

Hopkins scientists were able to successfully initiate nerve regeneration in rats researchers reported Monday at the 223rd national meeting of the American Chemical Society.

Dr. Ronald Schnaar, professor of pharmacology and neuroscience at Johns Hopkins University Medical School, lead the study which may help provide the knowledge base for discoveries in human never regeneration to treat spinal cord injuries and diseases such as multiple sclerosis and Parkinson's.

"In this study we have found one of the key players in the process by which nerves get the signal not to regenerate," said Schnaar, "by knowing that, we and others in the field can work together to develop technologies to enhance nerve regeneration."

Schnaar and collogues have found and identified four chemicals that caused damaged nerves to being regenerating. The experiments were conducted on cells in a petri dish, and thus this research has a long way to go before it could have any practical application to treating nerve diseases in humans.

Normal, healthy nerve cells are wrapped in an outer cellular sheet called myelin. Myelin acts like the insulation surrounding an electrical wire, and helps strengthen the electrical signal. Diseases such as multiple sclerosis are caused by a degeneration of the myelin sheet and thus a loss in nerve signal conductance.

"Myelin also has a dark side," Schnaar said. "When nerve axons are damaged, such as in spinal cord injuries, myelin stops them from regenerating. In large part, myelin blockade of axon regeneration is responsible for the lack of recovery from a nervous system injury."

During normal growth and development myelin cells make specific contacts with their axons and exchange molecular signals. Nerve cell injury however, disrupts these normal signaling pathways and causes the myelin to block the nerve cell from regenerating.

Despite the very promising results of his experiments, Schnaar cautioned, "nerve damage is very much more complex than our laboratory conditions and this new knowledge, by itself, is unlikely to provide aid to those suffering with nerve injury. However, it is our hope that our discoveries, along with other new discoveries on the molecular basis for nerve regeneration, will help in the search for therapies to improve functional recovery after nervous system injury or disease."

Rashmi Bansal, professor of neuroscience at the University of Connecticut Medical School in Farmington, told United Press International commented that Schnaar's research "is at the forefront of a current recognition of the fundamental importance of this class of lipids in biomedical science."

"There are important implications here for pathological situations, in particular nerve regeneration after injury or degenerative diseases, including multiple sclerosis, a disease in which nerve deterioration has recently been re-emphasized," Bansal added.

Schnaar is continuing his work to see if he can reproduce his findings in a living system, but he does not have preliminary results quite yet.

"We are getting at the mechanisms that underlie one of the problems in nerve regrowth but there are others," Schnaar said. "There is no magic formula for spinal cord repair."

Schnaar emphasized some of the difficulties in applying this knowledge about rat nerve cells to human cells.

"In the human body, nerve damage is much more complicated than it is in our laboratory conditions, and this new knowledge, by itself, is unlikely to solve the problem of nerve regeneration," says Schnaar. "However, it is our hope that our discoveries, along with other new discoveries on the molecular basis for nerve regeneration, will help in the search for therapies to improve functional recovery after nervous system injury or disease.


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