Scientists have identified a protein pathway that may help explain how aging contributes to neurodegenerative diseases, according to ScienceDaily.
The research team, led by Professor Dr. David Vilchez at the CECAD Cluster of Excellence for Aging Research, studied the tiny worm Caenorhabditis elegans to see how age-related changes affect harmful protein buildup. Their work focused on EPS8, an aging-associated protein that becomes more active over time.
According to the study, higher EPS8 activity promoted abnormal protein aggregation and neurodegeneration in worm models of Huntington’s disease and ALS. When researchers reduced EPS8 activity, toxic protein clumps were less likely to form and neuronal function was better preserved.
The team also tested the mechanism in human cell models of Huntington’s disease and ALS, where lowering EPS8 levels produced similar results. While the scientists say they still do not know exactly how EPS8 triggers aggregation, they believe the pathway could offer a target for future therapies.
