The Pathophysiological Role of Microglia in Dynamic Surveillance, Phagocytosis and Structural Remodeling of the Developing CNS
Open accessAbstract
In vertebrates, during an early wave of hematopoiesis in the yolk sac between embryonic day E7.0 and E9.0, cells of mesodermal leaflet addressed to macrophage lineage enter in developing central nervous system (CNS) and originate the developing native microglial cells. Depending on the species, microglial cells represent 5-20% of glial cells resident in adult brain. Here, we briefly discuss some canonical functions of the microglia, i.e. cytokine secretion and functional transition from M1 to M2 phenotype. In addition, we review studies on the non-canonical functions of microglia such as regulation of phagocytosis, synaptic pruning, and sculpting postnatal neural circuits. In this latter context the contribution of microglia to some neurodevelopmental disorders is now well established. Nasu-Hakola disease is considered a primary microgliopathy with alterations of the DAP12-TREM2 signaling and removal of macromolecules and apoptotic cells followed by secondary microglia activation. In Rett syndrome Mecp2-/- microglia shows a substantial impairment of phagocytic ability, although the role of microglia is not yet clear. In a mouse model of Tourette syndrome, microglia abnormalities have also been described, and deficient microglia-mediated neuroprotection is obvious. Here we review the role of microglial cells in neurodevelopmental disorders without inflammation and on the complex role of microglia in developing CNS.
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Neuroglial cells serve as the first line of defense for the brain, recognizing pathogens, repairing damaged tissue, secreting neurotrophic factors, and producing chemokines and cytokines.
“The neuroglial cells serve as the first line of defense for the brain, not only by recognizing pathogens and repairing damaged tissue but also by secreting neurotrophic factors and producing chemokines and cytokines.267”
From Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential (2023) · cites this paper as [267]
The Molecular Markers (Phenotypes) section describes microglia recognizing pathogen-associated signals, promoting wound healing, and releasing neurotrophic factors. The Cytokine Release section documents cytokine secretion and expression of chemokines including MIP-1α and MCP-1. The source supports these roles for microglia, but the claim extends them to neuroglial cells generally; it does not establish that all neuroglial cells serve as the brain’s first line of defense. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSeveral other AD risk polymorphisms, such as the R47H TREM2 mutation, alter microglial phagocytic capacity, leading to reduced clearance of Aβ aggregates and neuronal decline.
“Several other polymorphisms implicated as risk factors in AD, such as the R47H TREM2 mutation, result in alterations to microglial phagocytic capacity that lead to reduced clearance of Aβ aggregates and neuronal decline [27, 28].”
From Heterozygous expression of the Alzheimer’s disease-protective PLCγ2 P522R variant enhances Aβ clearance while preserving synapses (2022) · cites this paper as [27]
The Phagocytosis section associates TREM2 mutations with AD risk, and the Neurodevelopmental Diseases section says that nonfunctional TREM2 or DAP12 in AD patients impairs amyloid engulfment and is associated with dementia. The copy does not establish that the specific R47H variant causes this impaired clearance or neuronal decline; its explicit R47H reference concerns ALS. No page numbers are available in the indexed copy. (LLM, conf=0.86)
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Microglia and Brain Disorders: The Role of Vitamin D and Its Receptor
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- Authors
- Arcuri, C., Mecca, C., Bianchi, R., Giambanco, I., & Donato, R.
- Affiliations
- University of Perugia (IT)
- Corresponding author
- Donato, Rosario
- Venue
- Frontiers in Molecular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2017-06-19
- Volume
- 10
- Pages
- 191-191
- ISSN
- 1662-5099 (ISSN-L)
- PMC
- PMC5474494
- OpenAlex
- W2624934104
- Cited by
- 279
- References
- 195
- Citations by year
- 2026: 19 · 2025: 37 · 2024: 35 · 2023: 30 · 2022: 40 · 2021: 37 · 2020: 35 · 2019: 21 · 2018: 21 · 2017: 4
- FWCI
- 2.14
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Molecular Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Ministero dell’Istruzione, dell’Università e della Ricerca (SIR RBSI 144EUA)
- Fondazione Cassa di Risparmio di Perugia (2014.0254.021)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- microglia, central nervous system development, microglial origin, yolk sac hematopoiesis, phagocytosis, synaptic pruning, M1/M2 microglial polarization, cytokine production, Nasu-Hakola disease, Rett syndrome, MeCP2, Tourette syndrome, neurodevelopmental disorders, neuroprotection
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