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Study suggests possible way to repair damaged nerve cells

COLUMBUS, Ohio The loss of fully functioning nerve cells is a hallmark of brain diseases such as Alzheimer's and Parkinson's. But new evidence in rats and mice suggests that these neurons could be saved.

The results hold promise for designing treatments that might help not only people with brain diseases, but also victims of severe spinal cord and brain injuries.

Researchers report in the current online issue of the Proceedings of the National Academy of Sciences that they were able to prevent the death of damaged neurons by neutralizing a specific protein the injured cells secreted. Neurons carry messages from the brain to the spinal cord and the rest of the body.

Damaged neurons are rendered useless by the physical interaction of two cellular proteins proNGF and p75, the researchers report. They learned that treating these injured cells with a proNGF antibody kept the proteins from interacting. In turn the neurons were saved from almost certain loss.

"Knowing how these proteins influence each other gives us a window of opportunity to design a drug that could keep them from interacting," said Sung Ok Yoon, a lead author of the study and assistant professor of molecular and cellular biochemistry at Ohio State University.

She conducted the study with fellow lead author Klaus Giehl, of the University of Texas Southwestern Medical Center in Dallas; Andrew Harrington, of Ohio State's Center for Molecular Neurobiology; Barbara Hempstead, of Cornell University; and researchers from Germany, London, and New York.

"Coming up with a compound that crosses the blood-brain barrier is difficult," Giehl said. "If we create a molecule to keep p75 and proNGF from binding, we may be able to develop a therapy for patients."

The researchers examined brain and spinal cord tissue from healthy rats and mice and compared them to tissue from injured animals.

They looked for signs of proNGF and p75 in e
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Contact: Sung Ok Yoon
Yoon.84@osu.edu
614-292-8542
Ohio State University
15-Mar-2004


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