ArticleJournal of neuroimmunology2008
Role of Erk1/2 activation in prion disease pathogenesis: absence of CCR1 leads to increased Erk1/2 activation and accelerated disease progression.
Article in Journal of neuroimmunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 28 citations in OpenAlex.
- PrPStem cell reports · 2026Article
- Distinct neuronal alterations distinguish two subtypes of sporadic Creutzfeldt-Jakob disease with shared dysfunctional pathways.The Journal of clinical investigation · 2026Article
- Extracellular Vesicles, Stem Cells and the Role of miRNAs in Neurodegeneration.Current neuropharmacology · 2022Review
- Neuroinflammation in Prion Disease.International journal of molecular sciences · 2021Review
- NMDA Receptor and L-Type Calcium Channel Modulate Prion Formation.Cellular and molecular neurobiology · 2021Article
- Microglia in Prion Diseases: Angels or Demons?International journal of molecular sciences · 2020Review
- MAP/ERK Signaling in Developing Cognitive and Emotional Function and Its Effect on Pathological and Neurodegenerative Processes.International journal of molecular sciences · 2020Review
- GPI-anchor signal sequence influences PrPC sorting, shedding and signalling, and impacts on different pathomechanistic aspects of prion disease in mice.PLoS pathogens · 2019Article
- Microglia in prion diseases.The Journal of clinical investigation · 2017Review
- The Role of Unfolded Protein Response and Mitogen-Activated Protein Kinase Signaling in Neurodegenerative Diseases with Special Focus on Prion Diseases.Frontiers in aging neuroscience · 2017Review
- Distribution of Misfolded Prion Protein Seeding Activity Alone Does Not Predict Regions of Neurodegeneration.PLoS biology · 2016Article
- Prion Strain Differences in Accumulation of PrPSc on Neurons and Glia Are Associated with Similar Expression Profiles of Neuroinflammatory Genes: Comparison of Three Prion Strains.PLoS pathogens · 2016Article
- Insights into Mechanisms of Chronic Neurodegeneration.International journal of molecular sciences · 2016Review
- Cellular prion protein (PrP(C)) and its role in stress responses.International journal of clinical and experimental medicine · 2015Article
- The immunobiology of prion diseases.Nature reviews. Immunology · 2013Review
- Pathogenic prions deviate PrP(C) signaling in neuronal cells and impair A-beta clearance.Cell death & disease · 2013Article
- Early cytokine elevation, PrPres deposition, and gliosis in mouse scrapie: no effect on disease by deletion of cytokine genes IL-12p40 and IL-12p35.Journal of virology · 2012Article
- The immunology of neurodegeneration.The Journal of clinical investigation · 2012Review
- Engulfment of cerebral apoptotic bodies controls the course of prion disease in a mouse strain-dependent manner.The Journal of experimental medicine · 2010Article
- Analysis of protein levels of 24 cytokines in scrapie agent-infected brain and glial cell cultures from mice differing in prion protein expression levels.Journal of virology · 2009Article
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 1 country.
Funding
Abstract
Prion diseases are neurodegenerative infections with gliosis and vacuolation. The mechanisms of degeneration remain unclear, but chemokines may be important. In current experiments CCR1 knock-out (KO) mice succumbed more rapidly to scrapie infection than WT controls. Infected KO mice had upregulation of CCL3, a CCR1 ligand, and CCR5, a receptor with specificity for CCL3. Both infected KO and WT mice had upregulation of CCR5-mediated signaling involving activation of Erk1/2 in astrocytes; however, activation was earlier in KO mice suggesting a role in pathogenesis. In both mouse strains activation of the Erk1/2 pathway may lead to astrocyte dysfunction resulting in neurodegeneration.
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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.