ArticleGlia2014
Differential role of CCR2 in the dynamics of microglia and perivascular macrophages during prion disease.
Article in Glia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 60 citations in OpenAlex.
- Article
- Interleukin-1 regulates myeloid cell trafficking and cerebral blood flow following intracerebral haemorrhage.Disease models & mechanisms · 2025Article
- Knockout of P2Y12 receptor facilitates neuronal envelopment by reactive microglia and accelerates prion disease.Journal of neuroinflammation · 2025Article
- Dissecting surveying behavior of reactive microglia under chronic neurodegeneration.bioRxiv : the preprint server for biology · 2025Article
- Knockout of P2Y12 receptor facilitates microglia-neuron body-to-body interactions and accelerates prion disease.bioRxiv : the preprint server for biology · 2025Article
- Inhibiting CSF1R alleviates cerebrovascular white matter disease and cognitive impairment.Glia · 2024Article
- GSDMD in peripheral myeloid cells regulates microglial immune training and neuroinflammation in Parkinson's disease.Acta pharmaceutica Sinica. B · 2023Article
- Microglia deficiency accelerates prion disease but does not enhance prion accumulation in the brain.Glia · 2022Article
- Low-grade peripheral inflammation affects brain pathology in the AppActa neuropathologica communications · 2021Article
- Microglia as therapeutic targets after neurological injury: strategy for cell therapy.Expert opinion on therapeutic targets · 2021Review
- Neuroinflammation in Prion Disease.International journal of molecular sciences · 2021Review
- The Effects of Immune System Modulation on Prion Disease Susceptibility and Pathogenesis.International journal of molecular sciences · 2020Review
- The retinal environment induces microglia-like properties in recruited myeloid cells.Journal of neuroinflammation · 2019Article
- Prion pathogenesis is unaltered in a mouse strain with a permeable blood-brain barrier.PLoS pathogens · 2018Article
- Effect of chemokine CC ligand 2 (CCL2) on α‑synuclein‑induced microglia proliferation and neuronal apoptosis.Molecular medicine reports · 2018Article
- Systemic infection modifies the neuroinflammatory response in late stage Alzheimer's disease.Acta neuropathologica communications · 2018Article
- How do PrPPathogens (Basel, Switzerland) · 2017Review
- Microglia in prion diseases.The Journal of clinical investigation · 2017Review
- Microglia across the lifespan: from origin to function in brain development, plasticity and cognition.The Journal of physiology · 2017Review
- Lessons Learned about Neurodegeneration from Microglia and Monocyte Depletion Studies.Frontiers in aging neuroscience · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The expansion of the microglial population is one of the hallmarks of numerous brain disorders. The addition of circulating progenitors to the pool of brain macrophages can contribute to the progression of brain disease and needs to be precisely defined to better understand the evolution of the glial and inflammatory reactions in the brain. We have analyzed the degree of infiltration/recruitment of circulating monocytes to the microglial pool, in a prion disease model of chronic neurodegeneration. Our results indicate a minimal/absent level of CCR2-dependent recruitment of circulating monocytes, local proliferation of microglia is the main driving force maintaining the amplification of the population. A deficiency in CCR2, and thus the absence of recruitment of circulating monocytes, does not impact microglial dynamics, the inflammatory profile or the temporal behavioral course of prion disease. However, the lack of CCR2 has unexpected effects including the failure to recruit perivascular macrophages in diseased but not healthy CNS and a small reduction in microglia proliferation. These data define the composition of the CNS-resident macrophage populations in prion disease and will help to understand the dynamics of the CNS innate immune response during chronic neurodegeneration.
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What OpenQuestion holds
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.