Neurological conditions like Amyotrhophic lateral sclerosis (ALS) have long been linked to inflammation, but their association hasn’t been clear. Now, researchers at the Icahn School of Medicine at Mount Sinai have found a clue: They discovered that genetic changes may debilitate a protein linked to ALS, rendering it unable to moderate inflammation and thus exacerbate the progression of disease.

The study, published Monday in the journal Nature Immunology, analyzed the relationship of the protein, called senataxin, with the body’s antiviral response, according to a news release.

Scientists used genomic tools and gene expression studies to conclude that senataxin is released as part of the body’s natural antiviral response at a specific point, but when it doesn’t do its job, inflammation occurs. People with senataxin-related forms of ALS and ataxia possess a defective SETX gene that produces a disabled form of the protein, which suggests why inflammation is linked to them, and why the diseases progress.

Study co-author Harm van Bakel, an assistant genetics and genomic sciences professor at Mount Sinai, said in the news release that senataxin’s role with regards to its antiviral response had never been analyzed this extensively before. Previous research on the protein had been conducted in yeast cells, while this study analyzed human cells and animal models.

"This is a protein implicated in neurodegenerative disease that has now been linked to our innate antiviral mechanism, and it offers an intriguing clue to a relation between the inflammatory response and these diseases," study co-author Ivan Marazzi, an assistant microbiology professor at Mount Sinai, said in the news release. "Whether viral infection plays a role in disease progression remains to be seen, but this discovery has broad implications for biomedical research and opens up new avenues that we look forward to pursuing."