ArticleThe American journal of pathology2007
Microglial recruitment, activation, and proliferation in response to primary demyelination.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
118 citing papers in PubMed, 240 citations in OpenAlex.
- Teriflunomide Attenuates Demyelination and Enhances Remyelination in Organotypic Brain Slice Cultures Through Modulation of Glial Cell Dynamics.CNS neuroscience & therapeutics · 2026Article
- Niraparib Demonstrates Therapeutic Potential in Multiple Sclerosis through Inhibition of IL-17A Receptor Interaction and Promotion of Remyelination.ACS chemical neuroscience · 2025Article
- Apolipoprotein D Expression Dynamics During Cuprizone-Induced Demyelination and Remyelination in a Mouse Model of Multiple Sclerosis.International journal of molecular sciences · 2025Article
- Multiple sclerosis: what have we learned and can we still learn from electron microscopy.Cellular and molecular life sciences : CMLS · 2025Review
- Transcriptomic Analysis Divulges Differential Expressions of Microglial Genes After Microglial Repopulation in Mice.International journal of molecular sciences · 2025Article
- Alarm Functions of PD-1+ Brain-Resident Memory T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Neuroinflammation as a cause of differential Müller cell regenerative responses to retinal injury.Science advances · 2024Article
- Multisensory gamma stimulation mitigates the effects of demyelination induced by cuprizone in male mice.Nature communications · 2024Article
- Spatial dynamics of mammalian brain development and neuroinflammation by multimodal tri-omics mapping.bioRxiv : the preprint server for biology · 2024Article
- Spatiotemporal dynamics of the CD11cMolecular brain · 2024Article
- Exploring the Role of Apigenin in Neuroinflammation: Insights and Implications.International journal of molecular sciences · 2024Review
- Long-term in vivo three-photon imaging reveals region-specific differences in healthy and regenerative oligodendrogenesis.Nature neuroscience · 2024Article
- Roles in Innate Immunity.Advances in neurobiology · 2024Review
- Alzheimer's genes in microglia: a risk worth investigating.Molecular neurodegeneration · 2023Review
- Long-termbioRxiv : the preprint server for biology · 2023Article
- Localized Increased Permeability of Blood-Brain Barrier for Antibody Conjugates in the Cuprizone Model of Demyelination.International journal of molecular sciences · 2023Article
- Remyelination in animal models of multiple sclerosis: finding the elusive grail of regeneration.Frontiers in molecular neuroscience · 2023Review
- Cuprizone feeding induces swollen astrocyte endfeet.Pflugers Archiv : European journal of physiology · 2022Article
- Opposing effects of apoE2 and apoE4 on microglial activation and lipid metabolism in response to demyelination.Molecular neurodegeneration · 2022Article
- Review
58 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
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have characterized the cellular response to demyelination/remyelination in the central nervous system using the toxin cuprizone, which causes reproducible demyelination in the corpus callosum. Microglia were distinguished from macrophages by relative CD45 expression (CD45(dim)) using flow cytometry. Their expansion occurred rapidly and substantially outnumbered infiltrating macrophages and T cells throughout the course of cuprizone treatment. We used bromodeoxyuridine incorporation and bone marrow chimeras to show that both proliferation and immigration from blood accounted for increased microglial numbers. Microglia adopted an activated phenotype during demyelination, up-regulating major histocompatibility class I and B7.2/CD86. A subpopulation of CD45(dim-high) microglia that expressed reduced levels of CD11b emerged during demyelination. These microglia expressed CD11c and were potent antigen-presenting cells in vitro. T cells were recruited to the demyelinated corpus callosum but did not appear to be activated. Our study highlights the role of microglia as a heterogeneous population of cells in primary demyelination, with the capacity to present antigen, proliferate, and migrate into demyelinated areas.
Indexed as
Identifiers
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.