ArticleExperimental neurobiology2013
Brain inflammation and microglia: facts and misconceptions.
Article in Experimental neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
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Who cites it
101 citing papers in PubMed, 186 citations in OpenAlex.
- Stem cells redirect the neuroinflammatory trajectory of primed microglia in an ovine chorioamnionitis model.Brain, behavior, & immunity - health · 2026Article
- Extracellular vesicles: Revolutionizing targeted therapy for ischemic stroke.Acta pharmaceutica Sinica. B · 2026Review
- Microglia-Derived Extracellular Vesicles from Alzheimer's Disease Patients Carry miRNAs Driving a Neuroinflammatory Response.Molecular neurobiology · 2026Article
- Physical confinement and phagocytic uptake induce persistent cell migration.Biology open · 2025Article
- Acute experimental colitis in 5xFAD Alzheimer's disease mice leads to enhanced monocyte infiltration into the brain accompanied by reduced β-amyloid deposition.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Physical confinement and phagocytic uptake induce directional migration.bioRxiv : the preprint server for biology · 2025Article
- Steady Moderate Exercise Confers Resilience Against Neurodegeneration and Neuroinflammation in a Mouse Model of Parkinson's Disease.International journal of molecular sciences · 2025Article
- Neuroprotective Effects of Eugenol Acetate Against Ischemic Stroke.Journal of inflammation research · 2025Article
- The role of probiotics, prebiotics, and postbiotics: cellular and molecular pathways activated on glial cells in Alzheimer's disease.Frontiers in neuroscience · 2025Review
- Hematopoietic Growth Factors Regulate the Entry of Monocytes into the Adult Brain via Chemokine Receptor CCR5.International journal of molecular sciences · 2024Article
- Bone marrow-derived myeloid cells transiently colonize the brain during postnatal development and interact with glutamatergic synapses.iScience · 2024Article
- Microglial apolipoprotein E particles contribute to neuronal senescence and synaptotoxicity.iScience · 2024Article
- Mesenchymal Stem Cell-Macrophage Crosstalk Provides Specific Exosomal Cargo to Direct Immune Response Licensing of Macrophages during Inflammatory Responses.Stem cell reviews and reports · 2024Article
- Unraveling the enigma: housekeeping geneFrontiers in psychiatry · 2024Article
- Food-derived Peptides as Promising Neuroprotective Agents: Mechanism and Therapeutic Potential.Current topics in medicinal chemistry · 2024Review
- Article
- Time course of neuroinflammation after human stroke - a pilot study using co-registered PET and MRI.BMC neurology · 2023Article
- Daytime Light Deficiency Leads to Sex- and Brain Region-Specific Neuroinflammatory Responses in a Diurnal Rodent.Cellular and molecular neurobiology · 2023Article
- Altered GABAergic, glutamatergic and endocannabinoid signaling is accompanied by neuroinflammatory response in a zebrafish model of social withdrawal behavior.Frontiers in molecular neuroscience · 2023Article
- Spatial Analysis of Neural Cell Proteomic Profiles Following Ischemic Stroke in Mice Using High-Plex Digital Spatial Profiling.Molecular neurobiology · 2022Article
41 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
the inflammation that accompanies acute injury has dual functionsbactericidal action and repair. Bactericidal functions protect damaged tissue from infection, and repair functions are initiated to aid in the recovery of damaged tissue. Brain injury is somewhat different from injuries in other tissues in two respects. First, many cases of brain injury are not accompanied by infection: there is no chance of pathogens to enter in ischemia or even in traumatic injury if the skull is intact. Second, neurons are rarely regenerated once damaged. This raises the question of whether bactericidal inflammation really occurs in the injured brain; if so, how is this type of inflammation controlled? Many brain inflammation studies have been conducted using cultured microglia (brain macrophages). Even where animal models have been used, the behavior of microglia and neurons has typically been analyzed at or after the time of neuronal death, a time window that excludes the inflammatory response, which begins immediately after the injury. Therefore, to understand the patterns and roles of brain inflammation in the injured brain, it is necessary to analyze the behavior of all cell types in the injured brain immediately after the onset of injury. Based on our experience with both in vitro and in vivo experimental models of brain inflammation, we concluded that not only microglia, but also astrocytes, blood inflammatory cells, and even neurons participate and/or regulate brain inflammation in the injured brain. Furthermore, brain inflammation played by these cells protects neurons and repairs damaged microenvironment but not induces neuronal damage.
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