ArticleBMC systems biology2012
Gene regulatory network analysis supports inflammation as a key neurodegeneration process in prion disease.
Article in BMC systems biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
- Time-dependent transcriptomic response to scrapie exposure in ovine MSC-derived neuron-like cells.Frontiers in cellular and infection microbiology · 2026Article
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- GeneSetCart: assembling, augmenting, combining, visualizing, and analyzing gene sets.GigaScience · 2025Article
- Interactions between Cytokines and the Pathogenesis of Prion Diseases: Insights and Implications.Brain sciences · 2024Review
- Single_cell_GRN: gene regulatory network identification based on supervised learning method and Single-cell RNA-seq data.BioData mining · 2022Article
- RETRACTED: Neuroinflammatory Markers: Key Indicators in the Pathology of Neurodegenerative Diseases.Molecules (Basel, Switzerland) · 2022Review
- Bioinformatics and System Biology Techniques to Determine Biomolecular Signatures and Pathways of Prion Disorder.Bioinformatics and biology insights · 2022Article
- Article
- Novel Morphological Glial Alterations in the Spectrum of Prion Disease Types: A Focus on Common Findings.Pathogens (Basel, Switzerland) · 2021Article
- Neuropathology of Animal Prion Diseases.Biomolecules · 2021Review
- Regional Differences in Neuroinflammation-Associated Gene Expression in the Brain of Sporadic Creutzfeldt-Jakob Disease Patients.International journal of molecular sciences · 2020Article
- Core transcriptional regulatory circuits in prion diseases.Molecular brain · 2020Article
- Review
- Oxidative and Inflammatory Events in Prion Diseases: Can They Be Therapeutic Targets?Current aging science · 2019Review
- Discrimination of Prion Strain Targeting in the Central Nervous System via Reactive Astrocyte Heterogeneity in CD44 Expression.Frontiers in cellular neuroscience · 2019Article
- Expression of selected genes isolated from whole blood, liver and obex in lambs with experimental classical scrapie and healthy controls, showing a systemic innate immune response at the clinical end-stage.BMC veterinary research · 2018Article
- Cerebellar compartmentation of prion pathogenesis.Brain pathology (Zurich, Switzerland) · 2018Article
- Dietary magnesium and copper affect survival time and neuroinflammation in chronic wasting disease.Prion · 2016Article
- Application of "Omics" Technologies for Diagnosis and Pathogenesis of Neurological Infections.Current neurology and neuroscience reports · 2015Review
- Increased infectivity of anchorless mouse scrapie prions in transgenic mice overexpressing human prion protein.Journal of virology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe activation of immune cells in the brain is believed to be one of the earliest events in prion disease development, where misfolded PrionSc protein deposits are thought to act as irritants leading to a series of events that culminate in neuronal cell dysfunction and death. The role of these events in prion disease though is still a matter of debate. To elucidate the mechanisms leading from abnormal protein deposition to neuronal injury, we have performed a detailed network analysis of genes differentially expressed in several mouse prion models.
resultsWe found a master regulatory core of genes related to immune response controlling other genes involved in prion protein replication and accumulation, and neuronal cell death. This regulatory core determines the existence of two stable states that are consistent with the transcriptome analysis comparing prion infected versus uninfected mouse brain. An in silico perturbation analysis demonstrates that core genes are individually capable of triggering the transition and that the network remains locked once the diseased state is reached.
conclusionsWe hypothesize that this locking may be the cause of the sustained immune response observed in prion disease. Our analysis supports the hypothesis that sustained brain inflammation is the main pathogenic process leading to neuronal dysfunction and loss, which, in turn, leads to clinical symptoms in prion disease.
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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.