University of Cologne Identifies EPS8 Role in ALS, Huntington's; US PET Study Links Late-Onset Psychosis to Tau and Amy‑

A research team at the University of Cologne, led by Professor David Vilchez, reported that the aging‑associated protein EPS8 becomes hyper‑active in older organisms and drives toxic protein aggregation in models of amyotrophic lateral sclerosis (ALS) and Huntington’s disease. In Caenorhabditis elegans and cultured human cells, elevated EPS8 and RAC signaling promoted the formation of aggregates of mutant FUS, TDP‑43 and polyglutamine proteins, while genetic knock‑down of EPS8 or RAC prevented aggregation and preserved neuronal function.

In a separate study conducted in the United States, positron emission tomography (PET) imaging of patients experiencing first‑episode psychosis after age 40 revealed that roughly 65% showed abnormal tau protein accumulation and 35% displayed amyloid‑β positivity, compared with low rates in healthy older controls. The findings indicate that late‑onset psychosis often reflects underlying neurodegenerative pathology, with distinct tau distribution patterns in amyloid‑negative versus amyloid‑positive cases.