ArticleJournal of virology2018
Microglia Are Critical in Host Defense against Prion Disease.
Article in Journal of virology, 2018. 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.
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Who cites it
65 citing papers in PubMed, 98 citations in OpenAlex.
- Gpnmb defines a phagocytic state of microglia linked to cell death in prion disease mouse model.Nature communications · 2026Article
- Distinct neuronal alterations distinguish two subtypes of sporadic Creutzfeldt-Jakob disease with shared dysfunctional pathways.The Journal of clinical investigation · 2026Article
- Presymptomatic pharmacological inhibition of mGluR5 improves survival in a mouse model of prion diseases.Acta neuropathologica communications · 2026Article
- APOE genotype differentially modulates prion pathology in a mouse model.Acta neuropathologica communications · 2026Article
- APOE Genotype Differentially Modulates Prion Pathology in a Mouse Model.Research square · 2025Article
- Knockout of P2Y12 receptor facilitates neuronal envelopment by reactive microglia and accelerates prion disease.Journal of neuroinflammation · 2025Article
- Microglia-specific NF-κB signaling is a critical regulator of prion-induced glial inflammation and neuronal loss.PLoS pathogens · 2025Article
- Downregulation of STAT3 transcription factor reverses synaptotoxic phenotype of reactive astrocytes associated with prion diseases.Acta neuropathologica communications · 2025Article
- Balancing Microglial Density and Activation in Central Nervous System Development and Disease.Current issues in molecular biology · 2025Review
- Reactive Microglia and Astrocytes as Therapeutic Targets in Prion Diseases.Sub-cellular biochemistry · 2025Review
- Histamine stimulates human microglia to alter cellular prion protein expression via the HRH2 histamine receptor.Scientific reports · 2024Article
- NG2 glia protect against prion neurotoxicity by inhibiting microglia-to-neuron prostaglandin E2 signaling.Nature neuroscience · 2024Article
- Cell adhesion molecule CD44 is dispensable for reactive astrocyte activation during prion disease.Scientific reports · 2024Article
- Reactive astrocytes in prion diseases: Friend or foe?PLoS pathogens · 2024Review
- Review
- Interactions between Cytokines and the Pathogenesis of Prion Diseases: Insights and Implications.Brain sciences · 2024Review
- Excitatory neuron-prone prion propagation and excitatory neuronal loss in prion-infected mice.Frontiers in molecular neuroscience · 2024Article
- Article
- Non-human primates in prion diseases.Cell and tissue research · 2023Review
- Mechanisms of prion-induced toxicity.Cell and tissue research · 2023Review
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
5 authors at 1 institution in 1 country.
Funding
Abstract
Microglial cells in the central nervous system play important roles in neurodevelopment and resistance to infection, yet microglia can become neurotoxic under some conditions. An early event during prion infection is the activation of microglia and astrocytes in the brain prior to damage or death of neurons. Previous prion disease studies using two different strategies to manipulate signaling through the microglial receptor CSF-1R reported contrary effects on survival from prion disease. However, in these studies, reductions of microglial numbers and function were variable, thus confounding interpretation of the results. In the present work, we used oral treatment with a potent inhibitor of CSF-1R, PLX5622, to eliminate 78 to 90% of microglia from cortex early during the course of prion infection. Oral drug treatment early after infection with the RML scrapie strain significantly accelerated vacuolation, astrogliosis, and deposition of disease-associated prion protein. Furthermore, drug-treated mice had advanced clinical disease requiring euthanasia 31 days earlier than untreated control mice. Similarly, PLX5622 treatment during the preclinical phase at 80 days postinfection with RML scrapie also accelerated disease and resulted in euthanasia of mice 33 days earlier than infected controls. PLX5622 also accelerated clinical disease after infection with scrapie strains ME7 and 22L. Thus, microglia are critical in host defense during prion disease. The early accumulation of PrPSc in the absence of microglia suggested that microglia may function by clearing PrPSc, resulting in longer survival.
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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.