Led by Dr. Stefan Pulst—chair of the Department of Neurology—and Dr. Daniel Scoles—associate professor of neurology and study co-author—a new study suggests that some neurological disorders may share a protein: Staufen1.
According to “Protein Linked to ALS/Ataxia Could Play Key Role in Other Neurodegenerative Disorders,” a recent article from U Health, “Staufen1 has an important interaction with another protein called mTOR, a master regulator of many functions in the body that plays a key role in a process called autophagy. Autophagy, or ‘self-digestion,’ is a self-preservation mechanism that the body uses to remove dysfunctional cells.”
Additionally, the articles states that the findings connect Staufen1 to the “emerging concept that neurodegenerative diseases are linked to malfunctions in the way cells cope with cellular stress.” These findings also suggest that targeting Staufen1 could eventually lead to therapeutic interventions for a number of these disorders—potentially including ALS, cerebellar ataxia, Parkinson’s, and Huntington’s disease.
Drs. Pulst and Scoles mentioned that they are hopeful that “they can develop a medication to reduce Staufen1 levels in people at risk for sporadic ALS, the most common form of ALS, in which the causes of the disease are unknown.”
The article continues to state that “if lowering Staufen1 is effective for ALS, it could eventually lead to new therapeutic approaches for the treatment of Alzheimer’s disease and other Staufen1-related disorders.”
Read the full article here.