Finally, we got our studies on rotenone-induced alpha-synuclein aggregation, and the effect of PREP inhibition on this, published. This project started already at 2011 , and the original aim was to use rotenone toxin model in mice and then treat the animals with a PREP inhibitor. Now published cellular data was supposed to be just a supporting data for animal results. However, the animal model turned out to be unrepeatable, and we got the results only from our cellular models.

In brief, PREP inhibition by KYP-2047 significantly improved the cell viability of alpha-synuclein overexpressing cells when stressed by rotenone. Moreover, this was not an antioxidant effect but the effect of reduced alpha-synuclein aggregation process. Full-text article is available in the Neuroscience Letters website until 17th of November.