ArticleNeurobiology of disease2009
Anti-PrP Mab 6D11 suppresses PrP(Sc) replication in prion infected myeloid precursor line FDC-P1/22L and in the lymphoreticular system in vivo.
Article in Neurobiology of disease, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- APOE genotype differentially modulates prion pathology in a mouse model.Acta neuropathologica communications · 2026Article
- APOE Genotype Differentially Modulates Prion Pathology in a Mouse Model.Research square · 2025Article
- Exploring immunotherapeutic strategies for neurodegenerative diseases: a focus on Huntington's disease and Prion diseases.Acta pharmacologica Sinica · 2025Review
- Therapeutic Trajectories in Human Prion Diseases.Sub-cellular biochemistry · 2025Review
- Prion therapeutics: Lessons from the past.Prion · 2022Review
- Ligands binding to the prion protein induce its proteolytic release with therapeutic potential in neurodegenerative proteinopathies.Science advances · 2021Article
- Absence of Apolipoprotein E is associated with exacerbation of prion pathology and promotes microglial neurodegenerative phenotype.Acta neuropathologica communications · 2021Article
- Vaccination with Prion Peptide-Displaying Polyomavirus-Like Particles Prolongs Incubation Time in Scrapie-Infected Mice.Viruses · 2021Article
- Passive Immunization With a Novel Monoclonal Anti-PrP Antibody TW1 in an Alzheimer's Mouse Model With Tau Pathology.Frontiers in aging neuroscience · 2021Article
- Immunotherapy against Prion Disease.Pathogens (Basel, Switzerland) · 2020Review
- Anti-prion Protein Antibody 6D11 Restores Cellular Proteostasis of Prion Protein Through Disrupting Recycling Propagation of PrPMolecular neurobiology · 2019Article
- Antioxidant peroxiredoxin 6 protein rescues toxicity due to oxidative stress and cellular hypoxia in vitro, and attenuates prion-related pathology in vivo.Neurochemistry international · 2015Article
- Article
- Modulation of amyloid precursor protein expression reduces β-amyloid deposition in a mouse model.Annals of neurology · 2014Article
- The immunobiology of prion diseases.Nature reviews. Immunology · 2013Review
- Blocking the interaction between apolipoprotein E and Aβ reduces intraneuronal accumulation of Aβ and inhibits synaptic degeneration.The American journal of pathology · 2013Article
- Differential molecular chaperone response associated with various mouse adapted scrapie strains.Neuroscience letters · 2013Article
- Immunotherapy in prion disease.Nature reviews. Neurology · 2013Review
- Could immunomodulation be used to prevent prion diseases?Expert review of anti-infective therapy · 2012Article
- Biochemical properties of highly neuroinvasive prion strains.PLoS pathogens · 2012Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
The pathogenesis of prion diseases is related to conformational transformation of cellular prion protein (PrP(C)) into a toxic, infectious, and self-replicating conformer termed PrP(Sc). Following extracerebral inoculation, the replication of PrP(Sc) is confined for months to years to the lymporeticular system (LRS) before the secondary CNS involvement results in occurrence of neurological symptoms. Therefore, replication of PrP(Sc), in the early stage of infection can be targeted by therapeutic approaches, which like passive immunization have limited blood-brain-barrier penetration. In this study, we show that 6D11 anti-PrP monoclonal antibody (Mab) prevents infection on a FDC-P1 myeloid precursor cell line stably infected with 22L mouse adapted scrapie strain. Passive immunization of extracerebrally infected CD-1 mice with Mab 6D11 resulted in effective suppression of PrP(Sc) replication in the LRS. Although, a rebound of PrP(Sc) presence occurred when the Mab 6D11 treatment was stopped, passively immunized mice showed a prolongation of the incubation period by 36.9% (pb0.0001) and a significant decrease in CNS pathology compared to control groups receiving vehicle or murine IgG. Our results indicate that antibody-based therapeutic strategies can be used, even on a short-term basis, to delay or prevent disease in subjects accidentally exposed to prions.
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