ArticleThe Journal of general virology2016
Knockout of fractalkine receptor Cx3cr1 does not alter disease or microglial activation in prion-infected mice.
Article in The Journal of general virology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- APOE genotype differentially modulates prion pathology in a mouse model.Acta neuropathologica communications · 2026Article
- Article
- APOE Genotype Differentially Modulates Prion Pathology in a Mouse Model.Research square · 2025Article
- Dissecting surveying behavior of reactive microglia under chronic neurodegeneration.bioRxiv : the preprint server for biology · 2025Article
- Limbic system synaptic dysfunctions associated with prion disease onset.Acta neuropathologica communications · 2024Article
- Absence of Apolipoprotein E is associated with exacerbation of prion pathology and promotes microglial neurodegenerative phenotype.Acta neuropathologica communications · 2021Article
- Neuroinflammation in Prion Disease.International journal of molecular sciences · 2021Review
- Microglia in Prion Diseases: Angels or Demons?International journal of molecular sciences · 2020Review
- Review
- Microglia in neurodegeneration.Nature neuroscience · 2018Review
- Inflammatory response of microglia to prions is controlled by sialylation of PrPScientific reports · 2018Article
- Cytoskeleton-Associated Risk Modifiers Involved in Early and Rapid Progression of Sporadic Creutzfeldt-Jakob Disease.Molecular neurobiology · 2018Article
- Microglia in prion diseases.The Journal of clinical investigation · 2017Review
- Statins are ineffective at reducing neuroinflammation or prolonging survival in scrapie-infected mice.The Journal of general virology · 2017Article
- Loss of Fractalkine Signaling Exacerbates Axon Transport Dysfunction in a Chronic Model of Glaucoma.Frontiers in neuroscience · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Microglial activation is a hallmark of the neuroimmunological response to Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis and prion disease. The CX3C chemokine axis consists of fractalkine (CX3CL1) and its receptor (CX3CR1); these are expressed by neurons and microglia respectively, and are known to modulate microglial activation. In prion-infected mice, both Cx3cr1 and Cx3cl1 are altered, suggesting a role in disease. To investigate the influence of CX3C axis signalling on prion disease, we infected Cx3cr1 knockout (Cx3cr1-KO) and control mice with scrapie strains 22L and RML. Deletion of Cx3cr1 had no effect on development of clinical signs or disease incubation period. In addition, comparison of brain tissue from Cx3cr1-KO and control mice revealed no significant differences in cytokine levels, spongiosis, deposition of disease-associated prion protein or microglial activation. Thus, microglial activation during prion infection did not require CX3C axis signalling.
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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.