Cited by 301Neuroinflammation and Neurodegeneration MechanismsPhagocytosis and Immune RegulationAutophagy in Disease and Therapy

Astrocytes and microglia play orchestrated roles and respect phagocytic territories during neuronal corpse removal in vivo

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Damisah, Eyiyemisi C., Hill, Robert A., Rai, Anupama, Chen, Fuyi, Rothlin, Carla V., Ghosh, Sourav, Grutzendler, Jaime·2020·Science Advances

Abstract

Astrocytes and microglia have specialized roles and display a coordinated response during corpse removal in the live brain.

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Registry

Crossref · 10.1126/sciadv.aba3239

Cites

53 of 53 references verified0 citation errors · 0 not checkable

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  • Plcg2 deficiency leads to a mild inactivation of microglia.

    “Considering that microglia depletion leads to compensatory upregulation of astrocytic genes and activity (26, 27), taken together these results strongly suggest that Plcg2 deficiency leads to a mild inactivation of microglia.”

    From Multi-omics analyses reveal novel effects of PLCγ2 deficiency in the mouse brain (2023) · cites this paper as [27]

    The citation is attached to the premise about microglia depletion, not the citing authors’ subsequent inference about Plcg2. In Results (“A multicellular astrocytic reaction is responsible for cell body removal in the absence of microglia”; page unavailable), the source reports a compensatory astrocytic response after microglia were eliminated. It does not report upregulation of astrocytic genes or test Plcg2 deficiency. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • In the AD and PD brain, both astrocytes and microglia acquire reactive, inflammatory phenotypes and can effectively phagocytose aggregated proteins and cell debris, as well as secrete various cytokines and inflammatory mediators.

    “In the AD and PD brain, both astrocytes and microglia acquire reactive, inflammatory phenotypes and can effectively phagocytose aggregated proteins and cell debris, as well as secrete various cytokines and inflammatory mediators [8–13].”

    From Crosstalk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates (2021) · cites this paper as [10]

    The Introduction and Discussion report that astrocytes and microglia remove dying neurons and cellular debris, supporting the debris-phagocytosis part of the claim. The paper does not establish this in AD or PD brains, or show that both cell types phagocytose aggregated proteins, acquire inflammatory phenotypes, or secrete cytokines and inflammatory mediators. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • Microglia and astrocytes are responsible for many inflammatory processes in affected brains, including phagocytosis of αSYN and Aβ aggregates, secretion of inflammatory mediators, and stimulation of the innate immune system.

    “Microglia and astrocytes are known to be responsible for many inflammatory processes in affected brains, including phagocytosis of αSYN and Aβ aggregates, secretion of inflammatory mediators, and stimulation of the innate immune system [8–12].”

    From Crosstalk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates (2021) · cites this paper as [10]

    The Introduction and Discussion report that microglia and astrocytes coordinate the phagocytic removal of dying neurons and their debris. They do not establish phagocytosis of αSYN or Aβ aggregates, secretion of inflammatory mediators, or stimulation of the innate immune system; the paper's findings concern neuronal corpse removal rather than that full list of inflammatory processes. (LLM, conf=0.87)

    Experimental — accuracy not yet measured
  • Damisah et al. found that microglia eliminated from mice using a CSF1R antagonist, after which neuronal cell death was induced, resulted in astrocytes engulfing material intended for microglia but degrading it at a slower rate.

    “Damisah et al. provide support for this in their recent study, where microglia were eliminated from mice using a CSF1R antagonists, after which neuronal cell death was induced. They found that astrocytes engulfed the material which was intended for microglia but degraded it at a slower rate [10].”

    From Crosstalk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates (2021) · cites this paper as [10]

    The Results section, “A multicellular astrocytic reaction is responsible for cell body removal in the absence of microglia” (page unavailable), confirms CSF1R-antagonist treatment, induced neuronal apoptosis, astrocytic compensation, and slower cell-body removal. It does not establish a slower rate of degradation specifically; the authors also speculate that astrocytes digest cell bodies piecemeal rather than fully engulfing them. (LLM, conf=0.87)

    Experimental — accuracy not yet measured
  • Astrocytes and microglia degrade dead cells in a very organized and specialized manner; microglia degrade neuronal dendrites, cell bodies, and nuclei while astrocytes phagocytose apoptotic bodies that are released from dying neurons.

    “A recent study showed that astrocytes and microglia degrade dead cells in a very organized and specialized manner; microglia degrade neuronal dendrites, cell bodies, and nuclei while astrocytes phagocytose apoptotic bodies that are released from the dying neurons [10].”

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Authors
Damisah, E. C., Hill, R. A., Rai, A., Chen, F., Rothlin, C. V., Ghosh, S., & Grutzendler, J.
Affiliations
  • Yale University (US)
  • Dartmouth College (US)
Corresponding author
Grutzendler, Jaime
Venue
Science Advances
Published
2020-06-26
Volume
6
Issue
26
Pages
eaba3239-eaba3239
ISSN
2375-2548 (ISSN-L)
OpenAlex
W3038112026
Cited by
301
References
53
Citations by year
2026: 34 · 2025: 43 · 2024: 56 · 2023: 57 · 2022: 45 · 2021: 52 · 2020: 14
FWCI
16.26
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Science Advances (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Funders
  • NIH Office of the Director (R01-NS0889734, R00-NS099469)
  • NIH Clinical Center (RF1-AG05825)
  • Neurosurgery Research and Education Foundation (14-002715/AANS)
  • NIH-NIAID (R01-AI089824)
  • NIH-NCI (R01-CA212376)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
astrocytes, microglia, efferocytosis, phagocytosis, brain homeostasis, aging, neurodegeneration
MeSH terms
Astrocytes, Cadaver, Humans, Neurons, Phagocytes, Microglia

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