Disabled Protein Plays Role in Progression of Some Forms of ALS, Study Finds

 – March 31, 2015  –– 

Neurological conditions like Amyotrophic 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. Study co-author Harm van Bakel, PhD, 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. "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," said study co-author Ivan Marazzi, PhD, an assistant microbiology professor at Mount Sinai

-Honoratus Van Bakel, PhD, Assistant Professor, Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai
-Ivan Marazzi, PhD, Assistant Professor, Microbiology, Icahn School of Medicine at Mount Sinai

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