Karl Frontzek

This study identifies GLUL upregulation and altered glutamate/glutamine metabolism in prion-infected skeletal muscle, distinct from other neurodegenerative diseases.

This study identifies genetic variants associated with clinical duration in sporadic CJD but finds no significant SNPs for age at onset.

This study identifies an H-latch conformational switch in PrPC that drives prion toxicity and shows that disrupting this switch can protect against prion-related neurodegeneration.

The paper develops a human iPSC-derived neural model to study TDP-43 pathology, identifying NPTX2 misregulation as a key factor in ALS/FTLD neurotoxicity.

The paper shows that ligands binding to PrPC induce its proteolytic release, which has neuroprotective effects, and identifies mechanisms and exceptions in this process.

The paper shows that loss of PIKfyve contributes to spongiform degeneration in prion diseases by linking prion infection to PIKfyve destabilization and vacuolation.

This paper shows that ASC controls AA amyloidosis by interacting with SAA and that anti-ASC antibodies reduce amyloid loads in mice.

This study uses longitudinal whole-brain imaging to show that anti-Aβ therapies have distinct spatial and temporal efficacies, with polythiophenes showing strong Aβ clearance.

The paper identifies protective anti-prion antibodies in human immunoglobulin repertoires and finds they are present in healthy individuals without associated pathologies.

This study shows that SARM1 deficiency accelerates prion disease progression by upregulating XAF1, leading to increased neuronal apoptosis.

This paper introduces a bispecific antibody that targets both the globular domain and flexible tail of PrP, preventing prion toxicity and oligomer formation.