http://insciences.org/article.php?article_id=7908&utm_source=feedburner&...

DALLAS – Researchers at UT Southwestern Medical Center have found that a molecule produced naturally by muscles in response to nerve damage can reduce symptoms and prolong life in a mouse model of amyotrophic lateral sclerosis (ALS).

“We believe we can apply this research toward drug development,” said Dr. Eric Olson, chairman of molecular biology at UT Southwestern and senior author of the study, which appears in the Dec. 11 issue of Science.

ALS, also known as Lou Gehrig’s disease, damages motor nerve cells that control muscles, leading to muscle weakness, paralysis and death. There is no treatment that can slow it, and no cure.

As ALS kills nerves, the muscles they control begin to wither. The damaged muscles, however, can “re-innervate” themselves by prompting healthy nerves to send new branches their way, like limbs in a damaged hedge filling in a gap.

Dr. Olson said skeletal muscles produce a molecule called microRNA-206 (miR-206) to serve as a chemical signal to steer the new nerve endings and maintain their interactions with muscles. But the research suggests that miR-206 can only work for so long. As nerves continue to die, there comes a point where the surviving nerves can no longer carry the load, and symptoms like muscle weakness appear.