A multi-center effort led by researchers at the University of California, San Diego (UCSD) School of Medicine, has determined in mouse models of amyotrophic lateral sclerosis (ALS) that the nerve cells, or neurons, involved in ALS can be either damaged or saved from degeneration by neighboring non-neuronal cells.

The team reports that when non-neuronal cells harbor a genetic mutation associated with ALS, also called Lou Gehrig's disease, they can cause damage in normal "motor neurons," the long and complex nerve cells that control voluntary movement. Degeneration of motor neurons in ALS leads to progressive loss of muscle control, paralysis and ultimately death.

However, when the neighboring non-neuronal cells are normal, they can protect or rescue motor neurons from degeneration when the neurons themselves carry the ALS mutation. Published in the October 3, 2003 issue of the journal Science, the findings implicate non-neuronal cells in the disease, suggesting the potential of stem cell replacement therapy targeting non-neuronal cells as a treatment for ALS.

"In place of the Herculean task of replacing the huge, meter-long motor neurons damaged by ALS, it would be easier to replace some of the surrounding cells with normal cells. Based on our findings, this could potentially prevent the degeneration and death of motor neurons that would otherwise be targeted for premature death," said senior author Don Cleveland, Ph.D., UCSD Professor of Medicine, Neurosciences and Cellular and Molecular Medicine and member of the Ludwig Institute for Cancer Research.

Co-senior author Lawrence S.B. Goldstein, Ph.D., UCSD Professor of Cellular and Molecular Medicine and a Howard Hughes Medical Institute investigator, added that "we still need to do more research, but our hope is that stem cell therapy might be a candidate to rescue support cells and treat ALS patients."

ALS is a progressive disease that attacks motor neurons that reach from
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Contact: Sue Pondrom
spondrom@ucsd.edu
619-543-6163
University of California - San Diego
2-Oct-2003

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