Cited by 88Neuroinflammation and Neurodegeneration MechanismsPhagocytosis and Immune RegulationAutophagy in Disease and Therapy

Phagocytic astrocytes: Emerging from the shadows of microglia

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Konishi, Hiroyuki, Koizumi, Schuichi, Kiyama, Hiroshi·2022·Glia

Abstract

Elimination of dead or live cells take place in both a healthy and diseased central nervous system (CNS). Dying or dead cells are quickly cleared by phagocytosis for the maintenance of a healthy CNS or for recovery after injury. Live cells or parts thereof, such as the synapses and myelin, are appropriately eliminated by phagocytosis to maintain or refine neural networks during development and adulthood. Microglia, the specific population of resident macrophages in the CNS, are classically considered as primary phagocytes; however, astrocytes have also been highlighted as phagocytes in the last decade. Phagocytic targets and receptors are reported to be mostly common between astrocytes and microglia, which raises the question of how astrocytic phagocytosis differs from microglial phagocytosis, and how these two phagocytic systems cooperate. In this review, we address the consequences of astrocytic phagocytosis, particularly focusing on these elusive points.

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  • Reactive astrocytes accumulating around Aβ plaques constitute a neuroprotective barrier to prevent Aβ neurotoxicity spreading and phagocytose Aβ plaques.

    “It has been suggested that reactive astrocytes accumulating around Aβ plaques constitute a neuroprotective barrier to prevent not only Aβ neurotoxicity spreading but also phagocytose Aβ plaques (Konishi et al., 2022).”

    From Cell Adhesion Molecule Protocadherin-γC5 Ameliorates Aβ Plaque Pathogenesis by Modulating Astrocyte Function in Alzheimer's Disease (2025) · cites this paper as Konishi et al., 2022

    The Conclusions and Future Perspectives section says astrocytes phagocytose Aβ and that enhancing astrocytic lysosomal biogenesis promotes Aβ clearance and ameliorates plaque pathology. It does not say that reactive astrocytes accumulate around plaques or form a neuroprotective barrier that prevents Aβ neurotoxicity from spreading; searches for those points found no supporting passage. Page numbers were not available in our copy. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • Accumulated reactive astrocytes surrounding Aβ plaques form a barrier to limit spreading of pathological Aβ and clear Aβ deposits through phagocytosis, exerting neuroprotective function in Alzheimer's disease.

    “accumulated reactive astrocytes have been commonly observed surrounding Aβ plaques, forming a barrier to limit the spreading of pathological Aβ in the brain parenchyma and clear Aβ deposits through phagocytosis, exerting neuroprotective function in AD (Verkhratsky et al., 2016;Preman et al., 2021;Konishi et al., 2022).”

    From Cell Adhesion Molecule Protocadherin-γC5 Ameliorates Aβ Plaque Pathogenesis by Modulating Astrocyte Function in Alzheimer's Disease (2025) · cites this paper as Konishi et al., 2022

    The Conclusions and Future Perspectives section says astrocytes phagocytose Aβ and reports that enhancing astrocytic lysosomal biogenesis promotes Aβ clearance and ameliorates plaque pathology in AD mouse models. It does not say that reactive astrocytes surrounding plaques form a barrier that limits Aβ spread, so that part of the attributed claim is unsupported. (LLM, conf=0.87)

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Authors
Konishi, H., Koizumi, S., & Kiyama, H.
Affiliations
  • Nagoya University (JP)
  • University of Yamanashi (JP)
Corresponding author
  • Konishi, Hiroyuki
  • Koizumi, Schuichi
  • Kiyama, Hiroshi
Venue
Glia
Publisher
Wiley
Published
2022-02-10
Volume
70
Issue
6
Pages
1009-1026
ISSN
  • 0894-1491 (ISSN-L)
  • 1098-1136
OpenAlex
W4210966520
Cited by
88
References
185
Citations by year
2026: 17 · 2025: 24 · 2024: 25 · 2023: 18 · 2022: 4
FWCI
1.81
Type
journal article
Language
en
Open access
Locations
  • Glia (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • Japan Agency for Medical Research and Development (JP21gm1310008)
  • Japan Science and Technology Agency (JPMJCR14G2)
  • Japan Society for the Promotion of Science (19H03395, 19H04746, 19K06904, 20H05060, 20H05902, 21H04786, 21K19309)
  • Mitsubishi Foundation
  • Nakatomi Foundation
  • Takeda Science Foundation
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, phagocytosis, microglia, phagocytic receptors, synaptic pruning, myelin phagocytosis, central nervous system injury, brain development, central nervous system
MeSH terms
Astrocytes, Central Nervous System, Phagocytes, Phagocytosis, Microglia

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