Scientists may have found aging’s hidden trigger for brain disease
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- Researchers at the University of Cologne's CECAD Cluster of Excellence identified the protein EPS8 as a molecular switch that may explain why aging drives neurodegenerative diseases like ALS and Huntington's, publishing the findings in Nature Aging.
- In C. elegans worms, EPS8 accumulates with age and hyperactivates RAC signaling, promoting toxic protein clumping, neuronal damage, and shortened lifespan.
- First author Dr. Seda Koyuncu and colleagues demonstrated that reducing EPS8 activity blocked harmful protein aggregates and preserved nerve function in worm models of both Huntington's disease and ALS.
- The mechanism was conserved in human cells — lowering EPS8 levels in human Huntington's and ALS cell models similarly prevented toxic protein aggregate accumulation, according to the study.
- Professor Dr. David Vilchez, who led the research, noted the discovery fills a key gap in understanding how age-related molecular changes contribute to neurodegeneration.
- Scientists still do not know exactly how increased EPS8 activity causes proteins to aggregate, but EPS8 and its RAC signaling partners are now candidate targets for future therapies.
Why it matters: Aging remains the single strongest risk factor for ALS and Huntington's, yet no treatment targets the aging process itself. By pinning EPS8 and its RAC signaling pathway as a direct molecular bridge between getting older and toxic protein buildup — and showing the mechanism holds in human cells, not just worms — the study gives drug developers a concrete, evolutionarily conserved target that could eventually slow multiple neurodegenerative diseases at once rather than tackling each one separately.
