ArticleJournal of virology2002
Microglia from Creutzfeldt-Jakob disease-infected brains are infectious and show specific mRNA activation profiles.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
65 citing papers in PubMed, 123 citations in OpenAlex.
- Gpnmb defines a phagocytic state of microglia linked to cell death in prion disease mouse model.Nature communications · 2026Article
- Single-nucleus brain transcriptomics reveals microglia dysfunction in multiple system atrophy.Nature communications · 2026Article
- In Vitro Antioxidant and Anti-Neuroinflammatory Effects ofLife (Basel, Switzerland) · 2025Article
- Article
- Review
- Adipose-derived mesenchymal stromal cells decrease prion-induced glial inflammation in vitro.Scientific reports · 2022Article
- Review
- Astrocyte in prion disease: a double-edged sword.Neural regeneration research · 2022Review
- THαβ Immunological Pathway as Protective Immune Response against Prion Diseases: An Insight for Prion Infection Therapy.Viruses · 2022Review
- Reduced Expression of Prion Protein With Increased Interferon-β Fail to Limit Creutzfeldt-Jakob Disease Agent Replication in Differentiating Neuronal Cells.Frontiers in physiology · 2022Article
- Article
- Neuroinflammation in Prion Disease.International journal of molecular sciences · 2021Review
- Cross-Linking Cellular Prion Protein Induces Neuronal Type 2-Like Hypersensitivity.Frontiers in immunology · 2021Article
- Microglia in Prion Diseases: Angels or Demons?International journal of molecular sciences · 2020Review
- Prion protein protects mice from lethal infection with influenza A viruses.PLoS pathogens · 2018Article
- Article
- Flow Cytometric Detection of PrPJournal of virology · 2018Article
- What Is Our Current Understanding of PrPPathogens (Basel, Switzerland) · 2017Review
- Article
- Microglia in prion diseases.The Journal of clinical investigation · 2017Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Neurons are often assumed to be the principal sites for replication of the infectious agents causing Creutzfeldt-Jakob disease (CJD), scrapie, and bovine spongiform encephalopathy because they express high levels of normal and pathological prion protein (PrP). However, isolated brain cell types have not been evaluated for either infection or gene expression. Microglia purified from CJD-infected mice showed infectivity comparable to that of starting brain homogenate but expressed approximately 50-fold less PrP. CJD-infected microglia also displayed morphological changes indicative of cellular activation. To determine the molecular pathways of activation, we evaluated pertinent transcripts, including those linked to inflammation. Semiquantitative reverse transcription-PCR showed a >4-fold increase in cathepsin S, an enzyme important in antigen presentation, the cytokine interleukin-1beta, and the chemokine B-lymphocyte chemoattractant. The profile of microglial changes induced by the CJD agent differed substantially from activation induced by bacterial lipopolysaccharide or by beta-amyloid, a structure comparable to pathological PrP. These microglial studies emphasize migratory hematopoietic cells in the dispersion, and possibly replication, of the CJD agent. The low PrP levels in these highly infectious and activated cells further support the concept that pathological PrP is the result of infection rather than the infectious agent itself. Because microglia develop a specific pattern of responses to the CJD agent, microglial markers may be exploited in the diagnosis of these spongiform encephalopathies.
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Registered trials
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.