ArticlePloS one2008
Effective gene therapy in a mouse model of prion diseases.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- A self-complementary recombinant adeno-associated virus vector coding for an anchorless prion protein carrying the G127V mutation extends survival in a rodent prion disease model.PLoS pathogens · 2026Article
- A self-complementary recombinant adeno-associated virus vector coding for an anchorless prion protein carrying the G127V mutation extends survival in a rodent prion disease model.bioRxiv : the preprint server for biology · 2026Article
- Recombinant ovine prion protein can be mutated at position 136 to improve its efficacy as an inhibitor of prion propagation.Scientific reports · 2023Article
- The Effect ofInternational journal of molecular sciences · 2022Article
- Low doses of bioherbicide favour prion aggregation and propagation in vivo.Scientific reports · 2018Article
- A dominant-negative mutant inhibits multiple prion variants through a common mechanism.PLoS genetics · 2017Article
- A Fluorescent Oligothiophene-Bis-Triazine ligand interacts with PrP fibrils and detects SDS-resistant oligomers in human prion diseases.Molecular neurodegeneration · 2016Article
- Article
- Treatment of Prion Disease with Heterologous Prion Proteins.PloS one · 2015Article
- The glial response to intracerebrally delivered therapies for neurodegenerative disorders: is this a critical issue?Frontiers in pharmacology · 2014Review
- Prion diseases and adult neurogenesis: how do prions counteract the brain's endogenous repair machinery?Prion · 2014Article
- Systemic delivery of siRNA down regulates brain prion protein and ameliorates neuropathology in prion disorder.PloS one · 2014Article
- A naturally occurring C-terminal fragment of the prion protein (PrP) delays disease and acts as a dominant-negative inhibitor of PrPSc formation.The Journal of biological chemistry · 2011Article
- Dominant prion mutants induce curing through pathways that promote chaperone-mediated disaggregation.Nature structural & molecular biology · 2011Article
- Feline immunodeficiency virus as a gene transfer vector in the rat nucleus tractus solitarii.Cellular and molecular neurobiology · 2010Article
- Insights into prion biology: integrating a protein misfolding pathway with its cellular environment.PrionArticle
- Review
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Classical drug therapies against prion diseases have encountered serious difficulties. It has become urgent to develop radically different therapeutic strategies. Previously, we showed that VSV-G pseudotyped FIV derived vectors carrying dominant negative mutants of the PrP gene are efficient to inhibit prion replication in chronically prion-infected cells. Besides, they can transduce neurons and cells of the lymphoreticular system, highlighting their potential use in gene therapy approaches. Here, we used lentiviral gene transfer to deliver PrPQ167R virions possessing anti-prion properties to analyse their efficiency in vivo. Since treatment for prion diseases is initiated belatedly in human patients, we focused on the development of a curative therapeutic protocol targeting the late stage of the disease, either at 35 or 105 days post-infection (d.p.i.) with prions. We observed a prolongation in the lifespan of the treated mice that prompted us to develop a system of cannula implantation into the brain of prion-infected mice. Chronic injections of PrPQ167R virions were done at 80 and 95 d.p.i. After only two injections, survival of the treated mice was extended by 30 days (20%), accompanied by substantial improvement in behaviour. This delay was correlated with: (i) a strong reduction of spongiosis in the ipsilateral side of the brain by comparison with the contralateral side; and (ii) a remarkable decrease in astrocytic gliosis in the whole brain. These results suggest that chronic injections of dominant negative lentiviral vectors into the brain, may be a promising approach for a curative treatment of prion diseases.
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