Amyotrophic lateral sclerosis, also known as Lou Gehrig’s disease or ALS, is a devastating, rapidly advancing disease of the nerve cells in the brain and spinal cord that control voluntary muscle movement. But researchers at NYU School of Medicine have identified a new target for slowing the deterioration of physical function for which the disease is so well known.

In their new study, published August 30, 2012 online ahead of print in Cell Reports, lead investigator Steven J. Burden, PhD, and colleagues show that, by increasing the signaling activity of a protein called muscle skeletal receptor tyrosine-protein kinase (MuSK), they were able to keep nerve cells attached to muscle longer into the progression of the disease in a mouse model of ALS.