Cited by 123Neuroinflammation and Neurodegeneration MechanismsNeuroscience and Neuropharmacology ResearchInflammasome and immune disorders

Microglial diversity by responses and responders

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Gertig, Ulla, Hanisch, Uwe-Karsten·2014·Frontiers in Cellular Neuroscience

Abstract

Microglia are the principal resident innate immune cells of the CNS. Their contributions to the normal development of the CNS, the maintenance and plasticity of neuronal networks and the safeguarding of proper functionality are becoming more and more evident. Microglia also survey the tissue homeostasis to respond rapidly to exogenous and endogenous threats, primarily with a protective outcome. However, excessive acute activation, chronic activity or an improper adaptation of their functional performance can foster neuropathologies. A key to the versatile response behavior of these cells is their ability to commit to reactive phenotypes, which reveal enormous complexity. Yet the respective profiles of induced genes and installed functions may build up on heterogeneous contributions of cellular subsets. Here, we discuss findings and concepts that consider the variety of microglial activities and response options as being based-at least in part-on a diversity of the engaged cells. Whether it is the production of proinflammatory cytokines, clearance of tissue debris, antigen presentation or the ability to sense neurotransmitters, microglial cells present with an unanticipated heterogeneity of their constitutive and inducible features. While the organizational principles of this heterogeneity are still largely unknown, functional implications are already perceptible.

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Crossref · 10.3389/fncel.2014.00101

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  • In AD, brain microglial cells are activated in response to Aβ and other neuropathological changes and undergo complex neuroinflammation processes, playing either a protective or detrimental role.

    “In AD, brain microglial cells are activated in response to Aβ and other neuropathological changes and undergo complex neuroinflammation processes,54 playing either a protective or detrimental role in the disease.55, 56”

    From Acoustofluidic assembly of 3D neurospheroids to model Alzheimer's disease (2020) · cites this paper as [54]

    The Conclusion (page unavailable) says microglia show signs of activation in response to neuropathological events, and the paper describes complex inflammatory responses. It does not specifically establish activation by Aβ in Alzheimer’s disease. The protective-or-detrimental clause is attached to citations 55 and 56, not this source. (LLM, conf=0.82)

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Authors
Gertig, U., & Hanisch, U.-K.
Affiliations
University of Göttingen (DE)
Corresponding author
Hanisch, Uwe-Karsten
Venue
Frontiers in Cellular Neuroscience
Published
2014-04-01
Volume
8
Pages
101-101
ISSN
1662-5102 (ISSN-L)
OpenAlex
W1968597551
Cited by
123
References
78
Citations by year
2026: 2 · 2025: 2 · 2024: 4 · 2023: 5 · 2022: 10 · 2021: 9 · 2020: 11 · 2019: 12 · 2018: 6 · 2017: 18 · 2016: 13 · 2015: 23 · 2014: 8
FWCI
1.67
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Frontiers in Cellular 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, cc-by-sa)
  • GoeScholar The Publication Server of the Georg-August-Universität Göttingen (Georg-August-Universität Göttingen) (submittedVersion, cc-by)
Funders
Deutsche Forschungsgemeinschaft (SFB TRR 43, TRR-43)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Keywords
microglia, microglial heterogeneity, microglial activation, inflammatory cytokines, debris removal, antigen presentation, neurotransmitter detection, CNS homeostasis, neuroinflammation, neuropathology

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