Microglia Biology: One Century of Evolving Concepts
Open accessAbstract
Microglia were first recognized as a distinct cell population in the CNS one century ago. For a long time, they were primarily considered to be phagocytes responsible for removing debris during CNS development and disease. More recently, advances in imaging and genetics and the advent of single-cell technologies provided new insights into the much more complex and fascinating biology of microglia. The ontogeny of microglia was identified, and their functions in health and disease were better defined. Although many questions about microglia and their roles in human diseases remain unanswered, the prospect of targeting microglia for the treatment of neurological and psychiatric disorders is tantalizing.
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Microglia are the main phagocytes in the central nervous system.
“Microglia are the main phagocytes in the central nervous system (Prinz, Jung, and Priller 2019).”
From Changes of the Primary Cilia in Alzheimer's Disease Pathogenesis (2025) · cites this paper as Prinz, Jung, and Priller 2019
Microglia are intricately involved in the development of the neuronal architecture of the embryonic brain by phagocytosing excess or apoptotic neuronal progenitor cells, while supporting the survival, proliferation, migration, and maturation of other NPCs and neurons.
“Microglia are intricately involved in the development of the neuronal architecture of the embryonic brain by phagocytosing excess or apoptotic neuronal progenitor cells (NPCs), while supporting the survival, proliferation, migration, and maturation of other NPCs and neurons ( Figure 1 Top) (13, 24).”
From The role of microglia in multiple sclerosis: implications for treatment with Bruton’s tyrosine kinase inhibitors (2025) · cites this paper as [24]
Microglial cells originate in the yolk sac and migrate to the developing brain at approximately the same time as neurons develop and before other glia appear.
“Microglial cells originate in the yolk sac and migrate to the developing brain at approximately the same time as the development of neurons is taking place, and before the appearance of other types of glia (13, 24).”
From The role of microglia in multiple sclerosis: implications for treatment with Bruton’s tyrosine kinase inhibitors (2025) · cites this paper as [24]
During embryonic development, microglia display amoeboid morphology, have high proliferation rates, and are actively engaged in phagocytosis.
“During embryonic development, microglia display amoeboid morphology, have high proliferation rates, and are actively engaged in phagocytosis (24).”
From The role of microglia in multiple sclerosis: implications for treatment with Bruton’s tyrosine kinase inhibitors (2025) · cites this paper as [24]
Microglial cells perform a wide variety of functions, which demands a high degree of plasticity and adaptability.
“Microglial cells perform a wide variety of functions, which demands a high degree of plasticity and adaptability ( Figure 1 ) (13, 24, 25).”
From The role of microglia in multiple sclerosis: implications for treatment with Bruton’s tyrosine kinase inhibitors (2025) · cites this paper as [24]
Microglia are highly dynamic cells that constantly survey their microenvironment and communicate with other CNS cells, both of which require cytoskeletal remodeling.
“Further, microglia are highly dynamic cells that are constantly surveying their microenvironment and communicating with other CNS cells, both of which are functions that require cytoskeletal remodeling (Uhlemann et al., 2016; Prinz et al., 2019).”
From Deletion of the Alzheimer’s disease risk gene Abi3 locus results in obesity and systemic metabolic disruption in mice (2022) · cites this paper as Prinz et al., 2019
The normal protective role of microglia is disrupted in response to CNS damage, inducing microglia to proliferate as reactive microgliosis.
“That normal protective role is disrupted in response to CNS damage, inducing microglia to proliferate as reactive “microgliosis” [309].”
From Revisiting the Pathogenesis of X-Linked Adrenoleukodystrophy (2025) · cites this paper as [309]
Normal microglia can suppress neuroinflammation and protect brain tissue by releasing anti-inflammatory mediators such as IL-10 and TGFβ.
“Normal microglia can suppress neuroinflammation and protect brain tissue by releasing anti-inflammatory mediators, such as IL-10 and TGFβ (reviewed in [309]).”
From Revisiting the Pathogenesis of X-Linked Adrenoleukodystrophy (2025) · cites this paper as [309]
Microglia display diverse and dynamic phenotypic states and play roles in development, adulthood, aging, and diseases.
“Microglia display diverse and dynamic phenotypic states and play a plethora of roles in development, adulthood (homeostasis), aging and diseases (Butovsky and Weiner, 2018; Prinz et al., 2019; Thion and Garel, 2020).”
From What is a cell type and how to define it? (2022) · cites this paper as Prinz et al., 2019
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BackgroundInfluentialBlood–Brain Barrier Breakdown in Alzheimer’s Disease: Mechanisms and Targeted Strategies
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“Microglia are resident central nervous system (CNS) macrophages now appreciated to play key roles in regulation of synaptic connectivity and modulation of neural activity.(1,2) Microglia are also increasingly recognized as important cellular drivers of brain diseases, ranging from neurodegenerative diseases such as Al…”
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BackgroundMore than meets the eye: The role of microglia in healthy and diseased retina
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miR-124: A Promising Therapeutic Target for Central Nervous System Injuries and Diseases
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- Authors
- Prinz, M., Jung, S., & Priller, J.
- Affiliations
- University of Freiburg (DE)
- Weizmann Institute of Science (IL)
- UK Dementia Research Institute (GB)
- Corresponding author
- Prinz, Marco
- Jung, Steffen
- Priller, Josef
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2019-10
- Volume
- 179
- Issue
- 2
- Pages
- 292-311
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2978969137
- Cited by
- 1,525
- References
- 197
- Citations by year
- 2026: 220 · 2025: 269 · 2024: 278 · 2023: 244 · 2022: 223 · 2021: 192 · 2020: 92 · 2019: 3 · 2013: 1 · 2012: 1
- FWCI
- 13.27
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 368 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- DZNE Pub (submittedVersion)
- Funders
- Sobek Foundation
- Ernst Jung Foundation
- German Research Foundation (SFB 992, SFB1160, Reinhart Koselleck grant, Ministry of Science, Research and Arts, Baden-Wuerttemberg)
- BMBF (AERIAL)
- Excellence Strategy (390939984)
- Israeli Science Foundation (887/11)
- European Research Council (Adv ERC 340345)
- International Progressive MS Alliance
- BIH
- DZNE
- UK DRI (Momentum Award)
- DFG (SFB/TRR167)
- 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, microglial phagocytosis, microglia-targeted therapy
- MeSH terms
- Animals, Homeostasis, Humans, Microglia, Neurodegenerative Diseases, Neurogenesis, Transcriptome
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