New targets for nerve diseases, nerve regrowth: It's all in the handshake

In this month's Proceedings of the National Academy of Sciences, scientists at Johns Hopkins and the National Institutes of Health describe an important piece in the puzzle of what can go wrong in nerve-damaging disorders such as multiple sclerosis and Guillian-Barre syndrome.

They've verified a previously suspected molecular bridge between nerve cells and their surroundings which, when broken, causes nerves to deteriorate in a way apparently identical to a variety of neurodegenerative diseases. The research adds new insight on nerve disease as well as a new focus for research on stimulating nerve cell regrowth in the brain and spinal cord.

Although the studies were performed in mice, "the human versions of the molecules involved are essentially identical in structure and type," says Ronald Schnaar, Ph.D., who led the research team; "we have no reason to believe the process in people would be significantly different."

In MS and other as-yet "unsolved" nervous system diseases, the spotlight has been on myelin, the insulating material that sheaths nerve cells in layers like a burrito wrap. In the disorders, the myelin sloughs off the surface of the nerve cell and beneath it, the axon -- the elongated part of the cell that relays messages -- disintegrates.

The new research focuses on a natural linkage -- or a "molecular handshake" as one researcher calls it -- between the myelin and the axon it insulates. The handshake isn't structurally important, the researchers say; it's not what holds the myelin in place, for example. But, as in such linkages that occur in immune cells, it apparently trips a series of reactions on either side that are necessary for normal nerve behavior.

The Hopkins/NIH researchers focused on one half of the handshake, on molecules called gangliosides that extend from the surface of the nerve cell membrane. Gangliosides are a family of complex carbohydrate and lipid-b

Contact: Marjorie Centofanti
Johns Hopkins Medical Institutions

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