Microglia in Health and Disease
Open accessAbstract
Microglia, the major myeloid cells of the central nervous system (CNS) are implicated in physiologic processes and in the pathogenesis of several CNS disorders. Since their initial description early in the 20th century, our ability to identify and isolate microglia has significantly improved and new research is providing insight into the functions of these cells in sickness and in health. Here, we review recent advances in our understanding of the role of microglia in physiological and pathological processes of the CNS with a focus on multiple sclerosis and Alzheimer's disease. Because of the prominent roles CX3CR1 and its ligand fractalkine played in bringing about these advances, we discuss the physiological and pathological roles of microglia as viewed from the CX3CR1-fractalkine perspective, providing a unique viewpoint. Based on the most recent studies of molecular profiling of microglia, we also propose a molecular and functional definition of microglia that incorporates the properties attributed to these cells in recent years.
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Microglia are the principal resident immune cells of the brain and participate in homeostasis and host defense against pathogens and CNS disorders.
“They are the principal resident immune cells of the brain and are involved in homeostasis and in host defense against pathogens and CNS disorders10,11.”
From Microglia in neurodegeneration (2018) · cites this paper as [11]
Targeted deletion of TAK1 in microglia in EAE reduced CNS inflammation and axonal and myelin damage via cell-autonomous inhibition of NF-κB, JNK, and ERK1/2.
“Targeted deletion of the transforming growth factor (TGF)-β-activated kinase 1 in microglia in EAE reduced CNS inflammation and axonal and myelin damage by cell-autonomous inhibition of the NF-κB, JNK, and ERK1/2 pathways11.”
From Microglia in neurodegeneration (2018) · cites this paper as [11]
Inflammation mediated by microglia can harm the brain.
“Microglia mediated inflammation can have deleterious consequences for the brain and much evidence indicates that microglial activation contributes to neurodegenerative disease such as AD, PD and ALD 40,41.”
From Efficient derivation of microglia-like cells from human pluripotent stem cells (2016) · cites this paper as [41]
Microglial activation contributes to neurodegenerative diseases such as AD, PD, and ALD.
“Microglia mediated inflammation can have deleterious consequences for the brain and much evidence indicates that microglial activation contributes to neurodegenerative disease such as AD, PD and ALD 40,41.”
From Efficient derivation of microglia-like cells from human pluripotent stem cells (2016) · cites this paper as [41]
Fractalkine is released by neurons and its receptor is expressed by microglia, constituting a neuron-microglial signaling system.
“Fractalkine, involved in indirect neuroprotection, is released by neurons and the receptor is expressed by microglia, their interactions constituting a neuron-microglial signaling system (Ransohoff and El Khoury, 2015).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Ransohoff and El Khoury, 2015
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Self-citation
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- Authors
- Ransohoff, R. M., & Khoury, J. E.
- Affiliations
- Cleveland Clinic (US)
- Venue
- Cold Spring Harbor Perspectives in Biology
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2015-09-09
- Volume
- 8
- Issue
- 1
- Pages
- a020560
- ISSN
- 1943-0264 (ISSN-L)
- PMC
- PMC4691795
- OpenAlex
- W2203955786
- Cited by
- 303
- References
- 104
- Citations by year
- 2026: 11 · 2025: 14 · 2024: 28 · 2023: 24 · 2022: 35 · 2021: 49 · 2020: 43 · 2019: 26 · 2018: 22 · 2017: 30 · 2016: 18 · 2015: 3
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cold Spring Harbor Perspectives in Biology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (RF1AG051506)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- microglia, central nervous system, multiple sclerosis, Alzheimer's disease, CX3CR1, fractalkine, neuroinflammation, myeloid cells
- MeSH terms
- CX3C Chemokine Receptor 1, Alzheimer Disease, Central Nervous System Diseases, Humans, Multiple Sclerosis, Signal Transduction, Microglia, Receptors, Chemokine, Chemokine CX3CL1
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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