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Graduate School of Biomedical Sciences Division of Cellular and Molecular Biology Research Group Discovers that Immunosuppressant FK506 Stimulates Autophagy and Slows the Progression of Prion Diseases

A research team led by Nagasaki University Graduate School of Biomedical Sciences Division of Cellular and Molecular Biology Associate Professor Ryuichiro Atarashi, Professor Noriyuki Nishida, and graduate student Takehiro Nakagaki discovered that FK506 (tacrolimus), frequently used during transplants as an immunosuppressant, stimulates autophagy (a cellular mechanism which plays an important role in the breaking down of proteins and organelles within cells), decreasing the amount of abnormal prion protein that accumulates in prion-infected cells.

They also observed that incubation periods were longer for prion-infected model mice to which FK506 had been administered, and confirmed an increase in autophagy-related genes in the brains of the mice, and a decrease in abnormal prion proteins in presymptomatic brain tissue.

While some aspects of the relationship between FK506 and autophagy remain unclear, the team's research found that for the group to which FK506 was administered, microglial activation and spongiform degeneration normally seen in prion-infected brains was significantly suppressed.

These findings suggest that FK506 can decrease the amount of aggregate proteins such as abnormal prion proteins in patients with neurodegenerative diseases such as prion diseases by stimulating autophagy, slowing neurodegeneration.

These research results were published in the June 19, 2013 online bulletin "Autophagy".