ArticleBMC neuroscience2014
Microglial Cx3cr1 knockout reduces prion disease incubation time in mice.
Article in BMC neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Adipose tissue, systematic inflammation, and neurodegenerative diseases.Neural regeneration research · 2023Review
- Article
- Neuroinflammation in Prion Disease.International journal of molecular sciences · 2021Review
- Microglia in Prion Diseases: Angels or Demons?International journal of molecular sciences · 2020Review
- Region-specific glial homeostatic signature in prion diseases is replaced by a uniform neuroinflammation signature, common for brain regions and prion strains with different cell tropism.Neurobiology of disease · 2020Article
- SARM1 deficiency up-regulates XAF1, promotes neuronal apoptosis, and accelerates prion disease.The Journal of experimental medicine · 2019Article
- Region-Specific Response of Astrocytes to Prion Infection.Frontiers in neuroscience · 2019Article
- Microglia in neurodegeneration.Nature neuroscience · 2018Review
- Inflammatory response of microglia to prions is controlled by sialylation of PrPScientific reports · 2018Article
- Immunohistochemical and Molecular Investigations Show Alteration in the Inflammatory Profile of Multiple System Atrophy Brain.Journal of neuropathology and experimental neurology · 2018Article
- What Is Our Current Understanding of PrPPathogens (Basel, Switzerland) · 2017Review
- Article
- Microglia in prion diseases.The Journal of clinical investigation · 2017Review
- Pharmacological Modulation of Functional Phenotypes of Microglia in Neurodegenerative Diseases.Frontiers in aging neuroscience · 2017Review
- Knockout of fractalkine receptor Cx3cr1 does not alter disease or microglial activation in prion-infected mice.The Journal of general virology · 2016Article
- Fractalkine Receptor Deficiency Is Associated with Early Protection but Late Worsening of Outcome following Brain Trauma in Mice.Journal of neurotrauma · 2016Article
- Absence of CCL2 and CCL3 Ameliorates Central Nervous System Grey Matter But Not White Matter Demyelination in the Presence of an Intact Blood-Brain Barrier.Molecular neurobiology · 2016Article
- Article
- Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundMicroglia are resident mononuclear phagocytes of the brain that become activated in response to insults including neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease and prion disease. In the central nervous system the chemokine Cx3cl1 (Fractalkine) is expressed by neurons and its exclusive receptor Cx3cr1 is expressed solely on microglia. Cx3cl1/Cx3cr1 signalling is thought to maintain microglia in their resting state and disrupting this equilibrium may allow microglia to become activated. In prion disease, microglial proliferation has been suggested to contribute to overall disease progression, however, in different mouse models of neurodegeneration, loss of Cx3cr1 has been shown to either worsen or improve the phenotype depending on the paradigm.
resultsTo investigate the role of Cx3cl1/Cx3cr1 signalling in prion disease we infected Cx3cr1 null mice with three different strains of prions. Following challenge with Chandler/RML, ME7 and MRC2 prion strains, Cx3cr1 knockout mice showed highly significant reductions in incubation time. No differences were seen in the pattern and localisation of activated microglia in the brain or in the mRNA expression levels of chemokines/cytokines (Cxcl10, Il-12b, Il-1b, Arg-1 and Cxc3l1).
conclusionOur data suggest a protective role for Cx3cl1/Cx3cr1 cross-talk 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.