Erica Stuart

The paper identifies an alternatively misfolded PrP species, PrPAM, generated by PRNP mutations that may initially protect against prion replication, explaining delayed disease onset.

This paper demonstrates that delivering a protective prion protein variant via gene therapy extends survival in a prion disease mouse model.

This study investigates whether distinct α-synuclein strains contribute to clinical subtypes of multiple system atrophy (MSA) and finds no differences in strain properties between MSA-C and MSA-P.

This study shows that stochastic misfolding leads to the formation of distinct α-synuclein strains both in vitro and in vivo, resulting in different disease phenotypes.

The paper compares the interactomes of mouse and bank vole prion proteins in brain tissue to determine if differences in protein interactions explain the bank vole's susceptibility to prions.

This study shows that PrPC expression does not significantly affect α-synuclein strain propagation, neuroinvasion, or evolution in transgenic mice.

This study shows that knock-in mice with specific prion protein mutations spontaneously develop prion disease, producing atypical prion strains with similar properties regardless of mutation type.