Both are defining features of age-associated neurodegenerative conditions, including Huntington's disease and ALS. When the scientists reduced EPS8 activity, toxic protein aggregates no longer accumulated as readily. This allowed the researchers to determine whether the mechanism they observed in worms might also be relevant to human disease. Even so, the results address an important gap in neurodegenerative disease research by identifying a direct molecular connection between aging and neurodegeneration. Treatments aimed at this pathway could potentially slow or prevent the progression of ALS, Huntington's disease, and other brain disorders associated with aging.