Gerold Schmitt‐Ulms

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.

This study shows that tau deletion enhances synaptic weakening in male rats but not females, revealing sex-dependent effects on synaptic function and actin dynamics.

The paper investigates ER and perinuclear space dilations in prion-infected mice and identifies TRPV2 as a contributor to this phenomenon, which may relate to spongiform degeneration.

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 somatostatin reduces Aβ plaque formation in aged mice by inhibiting Aβ aggregation, independent of neprilysin.