Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (541 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The third type of glial cell, along with astrocytes and oligodendrocytes (which together form the macroglia). Microglia vary in appearance depending on developmental stage, functional state, and anatomical location; subtype terms include ramified, perivascular, ameboid, resting, and activated. Microglia clearly are capable of phagocytosis and play an important role in a wide spectrum of neuropathologies. They have also been suggested to act in several other roles including in secretion (e.g., of cytokines and neural growth factors), in immunological processing (e.g., antigen presentation), and in central nervous system development and remodeling.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Microglias; Microglial Cell; Cell, Microglial; Microglial Cells.
Where it fits in the MeSH classification
- Broader topics
- Neuroglia
Research landscape
PubMed indexes 35,857 records tagged with the MeSH heading “Microglia” (counts retrieved 2026-10-29). 16,581 of them (46.2%) were published from 2020 onward, and the busiest period so far is 2020 onward with 16,581 records.
Reviews account for 4,541 records (12.7%) and meta-analyses for 30. Randomized controlled trials number 24 (0.1%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,363 |
| 2000-2009 | 5,290 |
| 2010-2019 | 12,623 |
| 2020 onward | 16,581 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 4,541 | 12.7% |
| Meta-analyses | 30 | 0.1% |
| Randomized controlled trials | 24 | 0.1% |
Method: PubMed query "Microglia"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in neuroscience
Neuroscience draws on tools with different strengths: cellular and animal work can manipulate circuits directly, while human imaging and electrophysiology observe the living brain at lower resolution. Small imaging studies are prone to false positives, and findings in animals do not always carry over to people. Clinical neurology and psychiatry rely on trials and cohort studies whose outcomes are often symptom scales. Check the species, the sample size, how the outcome was measured and whether results were replicated.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Microglia and neuroinflammation: function, heterogeneity, and crosstalk | 2026 | Review article Design not recorded in structured metadata | 11 | cc by PMID 42243476 · DOI · PMC13314975 |
| Foamy microglia link oxylipins to disease progression in multiple sclerosis | 2026 | Research article Design not recorded in structured metadata | 11 | cc by PMID 42168651 · DOI · PMC13337515 |
| Human microglial transitions at the Aβ-tau inflection point associate with divergent pathways to dementia and resilience | 2026 | Research article Design not recorded in structured metadata | 9 | cc by PMID 42243549 · DOI · PMC13278961 |
Microglia and neuroinflammation: function, heterogeneity, and crosstalk [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Microglia, the resident innate immune cells of the central nervous system (CNS), are indispensable for maintaining brain homeostasis, conducting immune surveillance, and responding to injury.
- Closing excerpt
- The hub position of microglia within neuroinflammatory networks, together with their unique cellular characteristics, may unlock a promising frontier for the development of precision therapeutic strategies against neuroinflammatory disorders.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (202 words)
Microglia, the resident innate immune cells of the central nervous system (CNS), are indispensable for maintaining brain homeostasis, conducting immune surveillance, and responding to injury. Recent single-cell sequencing studies have revealed that activated microglia exhibit a spectrum of activation states that extend well beyond the classical proinflammatory/anti-inflammatory dichotomy, encompassing distinct subpopulations such as disease-associated microglia (DAMs), termed interferon-responsive microglia (IRMs), and lipid-droplet-accumulating microglia (LDAMs). Their remarkable plasticity enables microglia to adopt dual functional roles-either neuroprotective or neurotoxic-depending on the context of neuroinflammatory disease progression. Furthermore, microglia do not act in isolation but serve as central communicators within a dynamic cellular network of the CNS, interacting with neurons, astrocytes, oligodendrocytes, and peripheral immune cells to regulate processes such as synaptic pruning, inflammatory amplification, and myelin integrity and repair. This review provides a comprehensive overview of microglial origin, development, and classification, as well as the dynamic spectrum of microglial cellular states. Furthermore, we discuss the classical and latest mechanisms of microglia-mediated neuroinflammation and focus on the crosstalk between microglia and other cells of the CNS. The hub position of microglia within neuroinflammatory networks, together with their unique cellular characteristics, may unlock a promising frontier for the development of precision therapeutic strategies against neuroinflammatory disorders.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42243476 · DOI · PMC13314975
Foamy microglia link oxylipins to disease progression in multiple sclerosis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Multiple sclerosis (MS) is a chronic neuroinflammatory disease in which demyelinating white matter lesions accumulate and expand, driving irreversible disability.
- Closing excerpt
- Our findings implicate disturbed lipid metabolism in chronic MS pathology and suggest that foamy microglia/macrophages are an interesting cell type to target for progressive disease.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (174 words)
Multiple sclerosis (MS) is a chronic neuroinflammatory disease in which demyelinating white matter lesions accumulate and expand, driving irreversible disability. Here we identify a distinct population of foamy GPNMB+ microglia/macrophages associated with lesion expansion in secondary progressive MS. Using integrated lipidomic, transcriptomic, proteomic, chemical proteomic and histological analyses of human postmortem MS lesions, we show that lesions containing foamy microglia/macrophages exhibit disrupted lipid metabolism, lysosomal stress and markers associated with heightened phagocytosis and antigen presentation without classical pro-inflammatory signatures. These lesions are enriched for oxylipins, bismonoacylglycerolphosphates and cholesterol esters, and are associated with increased B cell infiltration and IgG1. Monoacylglycerol lipase (MAGL), a lipid-metabolizing enzyme enriched in lesions with foamy microglia/macrophages, emerged as a potential therapeutic target. Inhibition of MAGL promoted lesion recovery and reduced microgliosis in a mouse model of demyelination. Finally, oxylipins in cerebrospinal fluid correlate with the proportion of foamy lesions, suggesting potential biomarkers for progression. Our findings implicate disturbed lipid metabolism in chronic MS pathology and suggest that foamy microglia/macrophages are an interesting cell type to target for progressive disease.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42168651 · DOI · PMC13337515
Human microglial transitions at the Aβ-tau inflection point associate with divergent pathways to dementia and resilience [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Alzheimer's disease (AD) is not an inevitable outcome of pathology but a dynamic process shaped by how brain cells respond to amyloid-β (Aβ) and tau.
- Closing excerpt
- Together, these findings highlight divergent resilience-associated mechanisms in human aging and position microglial state transitions at the Aβ-tau interface as candidate points of resilience with potential therapeutic relevance.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (165 words)
Alzheimer's disease (AD) is not an inevitable outcome of pathology but a dynamic process shaped by how brain cells respond to amyloid-β (Aβ) and tau. To disentangle these responses, we combined spatial transcriptomics and single-nucleus RNA sequencing of the superior frontal cortex from octogenarians living with or without dementia and from cognitively intact centenarians with comparable Aβ accumulation. We identified six distinct tissue domains representing a spatial pathological continuum of AD, with a key inflection point marked by a shift from Aβ-associated inflammatory changes to tau-associated cellular programs. This transition was accompanied by a change in microglial states, from early inflammatory to late antigen-presenting phenotypes, termed early and late plaque-induced gene (PIG) programs. Resilient individuals showed distinct pathological patterns: octogenarians without dementia lacked late PIGs, whereas centenarians showed late PIG activation that was uncoupled from tau accumulation. Together, these findings highlight divergent resilience-associated mechanisms in human aging and position microglial state transitions at the Aβ-tau interface as candidate points of resilience with potential therapeutic relevance.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42243549 · DOI · PMC13278961
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Induction of a common microglia gene expression signature by aging and neurodegenerative conditions: a co-expression meta-analysis [4]
- Research article Genetic analysis of the human microglial transcriptome across brain regions, aging and disease pathologies [5]
- Research article Neuroinflammation across neurological diseases [6]
- Research article Decoding microglial immunometabolism: a new frontier in Alzheimer's disease research [7]
- Research article Elucidating the specific mechanisms of the gut-brain axis: the short-chain fatty acids-microglia pathway [8]
- Research article Microglia as hunters or gatherers of brain synapses [9]
References
- Zong S, Cui X, Wu S, Lu Z. Microglia and neuroinflammation: function, heterogeneity, and crosstalk. . 2026. PMID 42243476 · DOI · PMC13314975
- van der Vliet D, Di X, Shamorkina TM, Coulon-Bainier C, Pavlovic A, van der Vliet IACM, et al.. Foamy microglia link oxylipins to disease progression in multiple sclerosis. . 2026. PMID 42168651 · DOI · PMC13337515
- Lu A, Chen WT, Dalby M, Sainz Garcia D, Vanheusden M, de Vries LE, et al.. Human microglial transitions at the Aβ-tau inflection point associate with divergent pathways to dementia and resilience. . 2026. PMID 42243549 · DOI · PMC13278961
- Holtman IR, Raj DD, Miller JA, Schaafsma W, Yin Z, Brouwer N, et al.. Induction of a common microglia gene expression signature by aging and neurodegenerative conditions: a co-expression meta-analysis. Acta Neuropathol Commun. 2015. PMID 26001565 · DOI · PMC4489356
- Lopes KP, Snijders GJL, Humphrey J, Allan A, Sneeboer MAM, Navarro E, et al.. Genetic analysis of the human microglial transcriptome across brain regions, aging and disease pathologies. Nat Genet. 2022. PMID 34992268 · DOI · PMC9245609
- Shi FD, Yong VW. Neuroinflammation across neurological diseases. Science. 2025. PMID 40536983 · DOI
- Jung ES, Choi H, Mook-Jung I. Decoding microglial immunometabolism: a new frontier in Alzheimer's disease research. Mol Neurodegener. 2025. PMID 40149001 · DOI · PMC11948825
- Cao Q, Shen M, Li R, Liu Y, Zeng Z, Zhou J, et al.. Elucidating the specific mechanisms of the gut-brain axis: the short-chain fatty acids-microglia pathway. J Neuroinflammation. 2025. PMID 40400035 · DOI · PMC12093714
- Pereira-Iglesias M, Maldonado-Teixido J, Melero A, Piriz J, Galea E, Ransohoff RM, et al.. Microglia as hunters or gatherers of brain synapses. Nat Neurosci. 2025. PMID 39663381 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.