Hamza Arshad

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 shows that P4HB/PDIA1 modulates PrPC levels and prion replication by stabilizing PrPC and acting as a chaperone in CAD5 cells.

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.

The paper identifies key amino acid residues in bank vole prion protein (BVPrP) that enable it to act as a universal prion acceptor, revealing molecular mechanisms for cross-species prion replication.

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.