ArticleVirology journal2013
Brain microglia were activated in sporadic CJD but almost unchanged in fatal familial insomnia and G114V genetic CJD.
Article in Virology journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Peripheral Signatures of Multidimensional Pathology in Symptomatic and Asymptomatic Creutzfeldt-Jakob Disease.CNS neuroscience & therapeutics · 2026Article
- Interactions between Cytokines and the Pathogenesis of Prion Diseases: Insights and Implications.Brain sciences · 2024Review
- Microglia and Sleep Disorders.Advances in neurobiology · 2024Review
- Enhanced M-CSF/CSF1R Signaling Closely Associates with PrPMolecular neurobiology · 2022Article
- Activation of Innate Immunity and Autophagy in Brain Tissues with Prion Disease and Degradation of Abnormal PrPs in Cells - China's Studies.China CDC weekly · 2022Review
- Recent advances in the histo-molecular pathology of human prion disease.Brain pathology (Zurich, Switzerland) · 2019Review
- An In VivoMolecular neurobiology · 2018Article
- Article
- An in vivoAnnals of clinical and translational neurology · 2018Article
- Inhibition of IL-1β Signaling Normalizes NMDA-Dependent Neurotransmission and Reduces Seizure Susceptibility in a Mouse Model of Creutzfeldt-Jakob Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Remarkable increases of α1-antichymotrypsin in brain tissues of rodents during prion infection.Prion · 2017Article
- Microglia in prion diseases.The Journal of clinical investigation · 2017Review
- Increases of Galectin-1 and its S-nitrosylated form in the Brain Tissues of Scrapie-Infected Rodent Models and Human Prion Diseases.Molecular neurobiology · 2017Article
- The Role of Microglia in Prion Diseases: A Paradigm of Functional Diversity.Frontiers in aging neuroscience · 2017Review
- Low activity of complement in the cerebrospinal fluid of the patients with various prion diseases.Infectious diseases of poverty · 2016Article
- Re-infection of the prion from the scrapie‑infected cell line SMB-S15 in three strains of mice, CD1, C57BL/6 and Balb/c.International journal of molecular medicine · 2016Article
- Genetic and Transcriptomic Profiles of Inflammation in Neurodegenerative Diseases: Alzheimer, Parkinson, Creutzfeldt-Jakob and Tauopathies.International journal of molecular sciences · 2016Review
- Proteomics analyses for the global proteins in the brain tissues of different human prion diseases.Molecular & cellular proteomics : MCP · 2015Article
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Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMicroglial activations have been described in different subtypes of human prion diseases such as sporadic Creutzfeldt-Jakob disease (CJD), variant CJD, Kuru and Gerstmann-Sträussler-Scheinker disease (GSS). However, the situation of microglia in other genetic prion diseases such as fatal familial insomnia (FFI) and familial CJD remains less understood. The brain microglia was evaluated comparatively between the FFI, G114V and sCJD cases in the study.
methodsSpecific Western blots, immunohistochemical and immunofluorescent assays were used to detect the changes of microglia and ELISA tests were used for levels of inflammatory cytokines.
resultsWestern blots, immunohistochemical and immunofluorescent assays illustrated almost unchanged microglia in the temporal lobes of FFI and G114V gCJD, but obviously increased in those of sCJD. The Iba1-levels maintained comparable in six different brain regions of FFI and G114V cases, including thalamus, cingulate gyrus, frontal cortex, parietal cortex, occipital cortex and temporal cortex. ELISA tests for inflammatory cytokines revealed significantly up-regulated IL-1β, IL-6 and TNF-α in the brain homogenates from sCJD, but not in those from FFI and G114V gCJD.
conclusionData here demonstrates silent brain microglia in FFI and G114V gCJD but obviously increased in sCJD, which reflects various pathogenesis of different human prion diseases subtypes.
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