ALS, also known as Lou Gehrig's disease, destroys the nerve cells that control muscles. This leads to loss of mobility, difficulty in breathing and swallowing, and eventually death.

Riluzole, the sole medication approved in US to treat the disease, has only marginal benefits in patients.

Scientists have now discovered that when they reduced the activity of an enzyme called sodium-potassium ATPase or limited cells' ability to make copies of this enzyme, the disease's destruction of nerve cells stopped.

The enzyme maintains the proper balance of sodium and potassium in cells by ejecting charged sodium particles and taking in charged potassium particles, allowing cells to maintain an electrical charge across their outer membranes.

"We blocked the enzyme with digoxin," said senior author, Azad Bonni from the Washington University' School of Medicine, St Louis in US.

"This had a very strong effect, preventing the death of nerve cells that are normally killed in a cell culture model of ALS," Bonni added.

In mice with mutation for inherited ALS, those with only one copy of the gene for sodium-potassium ATPase survived an average of 20 days longer and were mobile than those with two copies of the gene.

The findings appeared online in the journal Nature Neuroscience.

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