The axonal transport velocity of prions is independent of prion formation.

Authors

Sam M Koshy, Jay Hrdlicka, Michael G Nichols, Anthony S Stender, Jack H Taylor, Joaquín Castilla, Jason C Bartz

Published in

PLoS pathogens. Volume 22. Issue 7. Pages e1014456. Jul 24, 2026. Epub Jul 24, 2026.

Abstract

Prion diseases are caused by PrPSc, the self-templating infectious conformation of the normal host-encoded prion protein, PrPC. Spread of PrPSc in the peripheral and central nervous system follows a highly predictable pattern consistent with slow axonal transport along defined neuroanatomical pathways. The rate of PrPSc transport, the contribution of prion strain diversity, and the requirement for prion conversion during transport are poorly understood, in part, due to a lack of direct measurement of PrPSc transport under defined conditions. Here, using a combination of live animal and sciatic nerve explant culture experiments, and determined the velocity of PrPSc ranged from rates consistent with both slow and fast axonal transport. Interestingly, transport of PrPSc was not dependent upon prion conversion as it was observed using prion strain and host combinations that do not support prion formation. The rate of PrPSc transport of prion strains and synthetic prions suggest that prions can use both slow and fast modes of axonal transport. Overall, converging lines of evidence suggest that prions are transported at a range of velocities consistent with both slow and fast axonal transport that is independent prion formation.

PMID:
42497239
Bibliographic data and abstract were imported from PubMed on 25 Jul 2026.

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