“We have gained a better understanding of how nerve cells can be protected against ALS. This opens up new targets for future therapies,” says Eva Hedlund, professor of neurochemistry at Stockholm University and head of the study.

The fatal disease amyotrophic lateral sclerosis (ALS) occurs when specific nerve cells, known as motor neurons, die and their connections—synapses—with skeletal muscles break down. However, a few groups of motor neurons are resistant to the disease, including those that control the muscles of the eye.

The study shows that resistant motor neurons do not react significantly to the disease when it is caused by a hereditary SOD1 mutation, probably because they have very high basal levels of several nerve-protecting factors, such as Engrailed-1 (En1), Parvalbumin (Pvalb), Cd63, and Galanin (Gal). En1 is a transcription factor, a kind of “switch” for genes, which controls which proteins are produced in the cell.