Dynamic Responses of Microglia in Animal Models of Multiple Sclerosis
Open accessAbstract
Microglia play an essential role in maintaining central nervous system (CNS) homeostasis, as well as responding to injury and disease. Most neurological disorders feature microglial activation, a process whereby microglia undergo profound morphological and transcriptional changes aimed at containing CNS damage and promoting repair, but often resulting in overt inflammation that sustains and propagates the neurodegenerative process. This is especially evident in multiple sclerosis (MS), were microglial activation and microglia-driven neuroinflammation are considered key events in the onset, progression, and resolution of the disease. Our understanding of microglial functions in MS has widened exponentially in the last decade by way of new tools and markers to discriminate microglia from other myeloid populations. Consequently, the complex functional and phenotypical diversity of microglia can now be appreciated. This, in combination with a variety of animal models that mimic specific features and processes of MS, has contributed to filling the gap of knowledge in the cascade of events underlying MS pathophysiology. The purpose of this review is to present the most up to date knowledge of the dynamic responses of microglia in the commonly used animal models of MS, specifically the immune-mediated experimental autoimmune encephalomyelitis (EAE) model, and the chemically-induced cuprizone and lysolecithin models. Elucidating the spectrum of microglial functions in these models, from detrimental to protective, is essential to identify emerging targets for therapy and guide drug discovery efforts.
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Microglia have previously been described to play pivotal roles in EAE disease progression.
“Importantly, microglia have previously been described to play pivotal roles in EAE disease progression (Plastini et al., 2020).”
From SYK coordinates neuroprotective microglial responses in neurodegenerative disease (2022) · cites this paper as Plastini et al., 2020
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TGF-β in Mice Ameliorates Experimental Autoimmune Encephalomyelitis in Regulating NK Cell Activity
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Corrigendum: Phagocytosis in the Brain: Homeostasis and Disease
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Flagged first, then by citations
Cited by
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The immunology of multiple sclerosis
Attfield, K. E., Jensen, L. T., Kaufmann, M., Friese, M. A., & Fugger, L. (2022) · Nature Reviews Immunology · doi:10.1038/s41577-022-00718-z · Cited by 380 · see citing works
SYK coordinates neuroprotective microglial responses in neurodegenerative disease
Ennerfelt, H., Frost, E. L., Shapiro, D. A., Holliday, C., Zengeler, K. E., Voithofer, G., Bolte, A. C., Lammert, C. R., Kulas, J. A., Ulland, T. K., et al. (2022) · Cell · doi:10.1016/j.cell.2022.09.030 · Cited by 329 · see citing works
“Importantly, microglia have previously been described to play pivotal roles in EAE disease progression (Plastini et al., 2020).”
Anti-Inflammatory Effects of GLP-1 Receptor Activation in the Brain in Neurodegenerative Diseases
Diz-Chaves, Y., Mastoor, Z., Spuch, C., González-Matías, L. C., & Mallo, F. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23179583 · Cited by 148 · see citing works
- Authors
- Plastini, M. J., Desu, H. L., & Brambilla, R.
- Affiliations
- University of Miami (US)
- Corresponding author
- Brambilla, Roberta
- Venue
- Frontiers in Cellular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2020-08-20
- Volume
- 14
- Pages
- 269-269
- ISSN
- 1662-5102 (ISSN-L)
- PMC
- PMC7468479
- OpenAlex
- W3066200180
- Cited by
- 48
- References
- 179
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 7 · 2023: 12 · 2022: 12 · 2021: 7
- FWCI
- 3.00
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Cellular Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- University of Southern Denmark Research Portal (University of Southern Denmark) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute of Neurological Disorders and Stroke
- National Multiple Sclerosis Society
- Fondazione Italiana Sclerosi Multipla
- 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, multiple sclerosis, microglial activation, neuroinflammation, experimental autoimmune encephalomyelitis, cuprizone model, animal models of multiple sclerosis, microglial heterogeneity, neurodegeneration, neuroprotection, therapeutic target
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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