Researchers identify DNA damage as a potential target for Huntington’s treatments

Scientists at Lawrence Berkeley National Laboratory have uncovered a previously overlooked mechanism in Huntington’s disease. The research shows that neurons affected by the condition suffer from an abnormal buildup of DNA double-strand breaks, which are not solely tied to the gene mutation responsible for the disorder. Instead, the faulty huntingtin protein appears to hinder the cell’s natural DNA repair systems, worsening damage over time. Experiments with mice—including those without the gene expansion—demonstrated that this damage correlates with disease symptoms, suggesting it plays a direct role in neurodegeneration. The findings propose that antioxidants could mitigate these breaks, potentially easing symptoms. While further testing in human cells is needed, the discovery opens a pathway for treatments that address repair failures rather than the underlying genetic defect. The work was supported by the National Institutes of Health and involved collaboration with Harvard’s public health researchers. If validated, this approach could represent a shift in how Huntington’s is managed clinically.