Cited by 71Neuroinflammation and Neurodegeneration MechanismsNeurogenesis and neuroplasticity mechanismsPluripotent Stem Cells Research

Human iPSC-derived glia models for the study of neuroinflammation

Open access
Stöberl, Nina, Maguire, Emily, Salis, Elisa, Shaw, Bethany, Hall-Roberts, Hazel·2023·Journal of Neuroinflammation

Abstract

Neuroinflammation is a complex biological process that plays a significant role in various brain disorders. Microglia and astrocytes are the key cell types involved in inflammatory responses in the central nervous system. Neuroinflammation results in increased levels of secreted inflammatory factors, such as cytokines, chemokines, and reactive oxygen species. To model neuroinflammation in vitro, various human induced pluripotent stem cell (iPSC)-based models have been utilized, including monocultures, transfer of conditioned media between cell types, co-culturing multiple cell types, neural organoids, and xenotransplantation of cells into the mouse brain. To induce neuroinflammatory responses in vitro, several stimuli have been established that can induce responses in either microglia, astrocytes, or both. Here, we describe and critically evaluate the different types of iPSC models that can be used to study neuroinflammation and highlight how neuroinflammation has been induced and measured in these cultures.

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  • Moving towards higher levels of iPSC model complexity is thought to improve the 'brain-like' authenticity of disease mechanisms, but little available evidence currently supports this idea.

    “While moving towards higher levels of iPSC model complexity is thought to improve the ‘brain-like’ authenticity of disease mechanisms, little available evidence currently supports this idea [403].”

    From Revisiting the Pathogenesis of X-Linked Adrenoleukodystrophy (2025) · cites this paper as [403]

    The Conclusion says increasing iPSC model complexity is assumed to improve the ‘brain-like’ authenticity of inflammatory responses, but that little evidence supports the assumption because cross-model comparisons are scarce. The citing sentence broadens this specific point about inflammatory responses to disease mechanisms generally. (LLM, conf=0.84)

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Authors
Stöberl, N., Maguire, E., Salis, E., Shaw, B., & Hall-Roberts, H.
Affiliations
UK Dementia Research Institute (GB)
Corresponding author
Stöberl, Nina
Venue
Journal of Neuroinflammation
Published
2023-10-10
Volume
20
Issue
1
Pages
231-231
ISSN
1742-2094 (ISSN-L)
OpenAlex
W4387514494
Cited by
71
References
152
Citations by year
2026: 30 · 2025: 27 · 2024: 12 · 2023: 2
FWCI
1.85
Type
journal article
Language
en
Open access
Locations
  • Journal of Neuroinflammation (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • ORCA Online Research @Cardiff (Cardiff University) (submittedVersion, other-oa)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • UK Dementia Research Institute (UK DRI-DSI2020-IPMAR)
  • GW4 BioMed MRC Doctoral Training Partnership
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pluripotent Stem Cells Research
Keywords
neuroinflammation, induced pluripotent stem cells, iPSC-derived microglia, iPSC-derived astrocytes, in vitro disease model, co-culture, brain organoids, xenotransplantation, conditioned medium, inflammatory stimuli, cytokines, chemokines, reactive oxygen species
MeSH terms
Neuroinflammatory Diseases, Animals, Astrocytes, Central Nervous System, Humans, Neuroglia, Microglia, Mice, Induced Pluripotent Stem Cells

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