Scientists may have found aging’s hidden trigger for brain disease — SkimNews
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- Professor Dr. David Vilchez and his team at the University of Cologne's CECAD Cluster of Excellence for Aging Research identified EPS8 as a protein that accumulates with age and drives neurodegeneration.
- The researchers found that EPS8 activates RAC signaling in C. elegans, and that this hyperactivation promotes toxic protein aggregation — a hallmark of Huntington's disease and ALS.
- Reducing EPS8 activity in worm models of Huntington's and ALS prevented harmful protein aggregates from forming and preserved neuronal function.
- The same intervention blocked toxic aggregate accumulation in human cell models of both diseases, suggesting the mechanism is evolutionarily conserved and relevant beyond nematodes.
- The study, published in Nature Aging (Vol. 5, Issue 9, 2025; DOI: 10.1038/s43587-025-00943-w), is titled 'The aging factor EPS8 induces disease-related protein aggregation through RAC signaling hyperactivation.'
- First author Dr. Seda Koyuncu said the work addresses a long-standing puzzle: while age is the strongest risk factor for neurodegeneration, the underlying molecular connection has remained largely unknown.
- The authors acknowledge the precise mechanism by which EPS8 hyperactivity causes aggregation is still unresolved, though EPS8 and its signaling partners are now flagged as potential therapy targets.
Why it matters: Aging is the single biggest risk factor for ALS, Huntington's, and related neurodegenerative diseases, yet no treatment targets the aging process itself. The study gives drug developers a concrete, evolutionarily conserved protein target — EPS8 and its RAC signaling partners — that was previously invisible in the aging-to-neurodegeneration chain. If future compounds can safely reduce EPS8 activity in human neurons, they could theoretically slow or block disease onset rather than just manage symptoms.
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