ArticleJournal of virology1999
Microglial activation varies in different models of Creutzfeldt-Jakob disease.
Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
39 citing papers in PubMed, 88 citations in OpenAlex.
- Peripheral Signatures of Multidimensional Pathology in Symptomatic and Asymptomatic Creutzfeldt-Jakob Disease.CNS neuroscience & therapeutics · 2026Article
- Redox mechanisms and their pathological role in prion diseases: The road to ruin.PLoS pathogens · 2023Review
- THαβ Immunological Pathway as Protective Immune Response against Prion Diseases: An Insight for Prion Infection Therapy.Viruses · 2022Review
- The role of microglia in prion diseases and possible therapeutic targets: a literature review.Prion · 2021Review
- Neuroinflammation in Prion Disease.International journal of molecular sciences · 2021Review
- Neurodegenerative Disease and the NLRP3 Inflammasome.Frontiers in pharmacology · 2021Review
- Microglia in Prion Diseases: Angels or Demons?International journal of molecular sciences · 2020Review
- In vitro Modeling of Prion Strain Tropism.Viruses · 2019Review
- The NLRP3-Caspase 1 Inflammasome Negatively Regulates Autophagy via TLR4-TRIF in Prion Peptide-Infected Microglia.Frontiers in aging neuroscience · 2018Article
- Microglia in prion diseases.The Journal of clinical investigation · 2017Review
- Altered CaActa neuropathologica communications · 2017Article
- Cystatin F is a biomarker of prion pathogenesis in mice.PloS one · 2017Article
- Prion pathogenesis is unaltered in the absence of SIRPα-mediated "don't-eat-me" signaling.PloS one · 2017Article
- Genetic and Transcriptomic Profiles of Inflammation in Neurodegenerative Diseases: Alzheimer, Parkinson, Creutzfeldt-Jakob and Tauopathies.International journal of molecular sciences · 2016Review
- Defining the Microglia Response during the Time Course of Chronic Neurodegeneration.Journal of virology · 2015Article
- Article
- The immunobiology of prion diseases.Nature reviews. Immunology · 2013Review
- Brain microglia were activated in sporadic CJD but almost unchanged in fatal familial insomnia and G114V genetic CJD.Virology journal · 2013Article
- Prion disease and the innate immune system.Viruses · 2012Review
- PrP 106-126 altered PrP mRNA gene expression in mouse microglia BV-2 cells.Virologica Sinica · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Progressive changes in host mRNA expression can illuminate crucial pathogenetic pathways in infectious disease. We examined general and specific approaches to mRNA expression in three rodent models of Creutzfeldt-Jakob disease (CJD). Each of these models displays distinctive neuropathology. Although mRNAs for the chemokine receptor CCR5, the lysosomal protease cathepsin S, and the pleiotropic cytokine transforming growth factor beta1 (TGF-beta1) were progressively upregulated in rodent CJD, the temporal patterns and peak magnitudes of each of these transcripts varied substantially among models. Cathepsin S and TGF-beta1 were elevated more than 15-fold in mice and rats infected with two different CJD strains, but not in CJD-infected hamsters. In rats, an early activation of microglial transcripts preceded obvious deposits of prion protein (PrP) amyloid. However, in each of the three CJD models, the upregulation of CCR5, cathepsin S, and TGF-beta1 was variable with respect to the onset of PrP pathology. These results show glial cell involvement varies as a consequence of the agent strain and species infected. Although neurons are generally assumed to be the primary sites for agent replication and abnormal PrP formation, microglia may be targeted by some agent strains. In such instances, microglia can both process PrP to become amyloid and can enhance neuronal destruction. Because microglia can participate in agent clearance, they may also act as chronic reservoirs of infectivity. Finally, the results here strongly suggest that TGF-beta1 can be an essential signal for amyloid deposition.
Indexed as
Identifiers
What OpenQuestion holds
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.