ArticlePLoS pathogens2018
Prion pathogenesis is unaltered in a mouse strain with a permeable blood-brain barrier.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Smart Nanodelivery Systems for Immunometabolic Modulation in Osteoarthritis.Exploration (Beijing, China) · 2026Review
- Targeting TREM2 signaling shows limited impact on cerebrovascular calcification.Life science alliance · 2025Article
- Reactive astrocytes associated with prion disease impair the blood brain barrier.Neurobiology of disease · 2023Article
- Reactive astrocytes associated with prion disease impair the blood brain barrier.bioRxiv : the preprint server for biology · 2023Article
- Novel regulators of PrPC biosynthesis revealed by genome-wide RNA interference.PLoS pathogens · 2021Article
- Pericytes regulate vascular immune homeostasis in the CNS.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Article
- mSphere of Influence: Clearing a Path for High-Resolution Visualization of Host-Pathogen InteractionsmSphere · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transmissible spongiform encephalopathies (TSEs) are caused by the prion, which consists essentially of PrPSc, an aggregated, conformationally modified form of the cellular prion protein (PrPC). Although TSEs can be experimentally transmitted by intracerebral inoculation, most instances of infection in the field occur through extracerebral routes. The epidemics of kuru and variant Creutzfeldt-Jakob disease were caused by dietary exposure to prions, and parenteral administration of prion-contaminated hormones has caused hundreds of iatrogenic TSEs. In all these instances, the development of postexposure prophylaxis relies on understanding of how prions propagate from the site of entry to the brain. While much evidence points to lymphoreticular invasion followed by retrograde transfer through peripheral nerves, prions are present in the blood and may conceivably cross the blood-brain barrier directly. Here we have addressed the role of the blood-brain barrier (BBB) in prion disease propagation using Pdgfbret/ret mice which possess a highly permeable BBB. We found that Pdgfbret/ret mice have a similar prion disease incubation time as their littermate controls regardless of the route of prion transmission. These surprising results indicate that BBB permeability is irrelevant to the initiation of prion disease, even when prions are administered parenterally.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.