FET family proteins consist of fused in sarcoma/translocated in liposarcoma 
(FUS/TLS), Ewing's sarcoma (EWS), and TATA-binding protein-associated factor 15 
(TAF15). Mutations in the copper/zinc superoxide dismutase (SOD1), TAR 
DNA-binding protein 43 (TDP-43), and FET family proteins are associated with the 
development of amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative 
disease. There is currently no cure for this disease and few effective 
treatments are available. Epidemiological studies indicate that the consumption 
of tea is associated with a reduced risk of developing neurodegenerative 
diseases. The results of this study revealed that components of a pu-erh tea 
extract (PTE) interacted with FET family proteins but not with TDP-43 or SOD1. 
PTE induced the degradation of FET family proteins but had no effects on TDP-43 
or SOD1. The most frequently occurring ALS-linked FUS/TLS mutant protein, R521C 
FUS/TLS, was also degraded in the presence of PTE. Furthermore, ammonium 
chloride, a lysosome inhibitor, but not lactacystin, a proteasome inhibitor, 
reduced the degradation of FUS/TLS protein by PTE. PTE significantly reduced the 
incorporation of R521C FUS/TLS into stress granules under stress conditions. 
These findings suggest that PTE may have beneficial health effects, including 
preventing the onset of FET family protein-associated neurodegenerative diseases 
and delaying the progression of ALS by inhibiting the cytoplasmic aggregation of 
FET family proteins.