Researchers pinpoint EPS8 as aging-linked trigger of neurodegenerative protein clumps

Scientists at the University of Cologne, headed by Professor David Vilchez, have uncovered a molecular mechanism that may explain why aging increases vulnerability to neurodegenerative diseases. Their work focused on the protein EPS8, which accumulates in older Caenorhabditis elegans and triggers hyperactive RAC signaling, leading to the clumping of disease-associated proteins. In worm models of ALS and Huntington’s disease, lowering EPS8 activity halted aggregate formation and maintained nerve cell health.

The researchers extended the observation to human cell models, where EPS8 reduction similarly blocked toxic protein buildup. Published in Nature Aging, the findings bridge a gap between age-related cellular changes and neurodegeneration, highlighting EPS8 and its signaling partners as promising drug targets. The study emphasizes the value of simple model organisms for uncovering pathways relevant to human brain disorders.