While it has been known for some time that a mutation in the superoxide dismutase 1 gene plays a role in some cases of amyotrophic lateral sclerosis, just how it works has been a mystery. A pair of articles published in Nature Neuroscience last month point an accusatory finger at glial cells with mutant SOD1 in the degeneration of neurons associated with the disease.

One group uncovered an SOD1-mediated pathway associated with neurotoxicity, while the other described an embryonic stem cell-based model that could be useful for screening ALS candidates.