Title |
Microglial Cx3cr1knockout reduces prion disease incubation time in mice
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Published in |
BMC Neuroscience, March 2014
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DOI | 10.1186/1471-2202-15-44 |
Pubmed ID | |
Authors |
Julia Grizenkova, Shaheen Akhtar, Sebastian Brandner, John Collinge, Sarah E Lloyd |
Abstract |
Microglia 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. |
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Unknown | 1 | 100% |
Demographic breakdown
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Members of the public | 1 | 100% |
Mendeley readers
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France | 1 | 2% |
Unknown | 45 | 98% |
Demographic breakdown
Readers by professional status | Count | As % |
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Student > Ph. D. Student | 23 | 50% |
Researcher | 10 | 22% |
Student > Bachelor | 3 | 7% |
Student > Master | 3 | 7% |
Professor | 2 | 4% |
Other | 1 | 2% |
Unknown | 4 | 9% |
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Biochemistry, Genetics and Molecular Biology | 8 | 17% |
Neuroscience | 6 | 13% |
Pharmacology, Toxicology and Pharmaceutical Science | 4 | 9% |
Medicine and Dentistry | 2 | 4% |
Other | 5 | 11% |
Unknown | 6 | 13% |