Microglial Phagocytosis of Live Neurons

Brown, Guy C.; Neher, Jonas J.

doi:10.1038/nrn3710

Cited by 853Neuroinflammation and Neurodegeneration MechanismsPhagocytosis and Immune RegulationAutophagy in Disease and Therapy

Microglial Phagocytosis of Live Neurons

Brown, Guy C., Neher, Jonas J.·2014·Nature Reviews Neuroscience

DOI 10.1038/nrn3710

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Abstract

Microglia, the brain's professional phagocytes, can remove dead and dying neurons as well as synapses and the processes of live neurons. However, we and others have recently shown that microglia can also execute neuronal death by phagocytosing stressed-but-viable neurons - a process that we have termed phagoptosis. In this Progress article, we discuss evidence suggesting that phagoptosis may contribute to neuronal loss during brain development, inflammation, ischaemia and neurodegeneration.

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During diseases or inflammatory challenges, microglia have been shown to phagocytize endangered or damaged but still viable cells, playing a role in accelerating degeneration.
“However, during diseases or inflammatory challenges, microglia have been shown to phagocytize endangered or damaged but still viable cells, playing a role in accelerating degeneration [77].”
From Risk mitigation of immunogenicity: a key to personalized retinal gene therapy (2021) · cites this paper as [77]
TREM2 may enable the phagocytosis by microglia of stressed but viable neurons (phagoptosis).
“The latter study suggested that TREM2 may enable the phagocytosis by microglia of stressed but viable neurons, a process termed phagoptosis (Brown and Neher, 2014).”
From Microglia in Alzheimer’s disease (2018) · cites this paper as Brown and Neher, 2014
Inflammatory stress and sub-lethal pathological insults can induce stressed-but-viable neurons to expose reversible eat-me signals such as phosphatidylserine or calreticulin, causing the neurons to be phagocytosed and killed by activated microglia via phagoptosis.
“inflammatory stress and sub-lethal pathological insults can induce stressed-but-viable neurons to expose reversible ‘eat-me’ signals such as phosphatidylserine or calreticulin, causing the neurons to be phagocytosed and killed by activated microglia via a process called phagoptosis8”
From Interplay between innate immunity and Alzheimer disease: APOE and TREM2 in the spotlight (2018) · cites this paper as [8]
In their state of high activation, microglial cells acquire an amoeboid morphology and act like macrophages, engulfing debris.
“In their state of high activation, microglial cells acquire an amoeboid morphology and act like macrophages, engulfing debris (Brown and Neher, 2014).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Brown and Neher, 2014

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“Microglia respond vigorously to cell surface markers of neuronal injury, externalized in response to excitotoxicity and other cellular stress (Brown and Neher, 2014).”
Background
Microglial phagocytosis in Alzheimer disease
Brown, G. C., St George-Hyslop, P., Paolicelli, R. C., & Lemke, G. (2026) · Nature Reviews Neurology · doi:10.1038/s41582-025-01162-y · Cited by 36 · see citing works
Self-citation
Risk mitigation of immunogenicity: a key to personalized retinal gene therapy
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Loss of Homeostatic Microglia Signature in Prion Diseases
Wang, Y., Hartmann, K., Thies, E., Mohammadi, B., Altmeppen, H., Sepulveda-Falla, D., Glatzel, M., & Krasemann, S. (2022) · Cells · doi:10.3390/cells11192948 · Cited by 12 · see citing works
“Since these studies did not lead to conclusive data about the role of microglia and their putative PrPSc-reducing function, another line of experiments was performed to address the impact of “eat me”-signals on neurons or “eat-me”-receptors on microglia on neuronal survival in prion pathophysiology [83].”
Result
Roles of Microglia in Synaptogenesis, Synaptic Pruning, and Synaptic Plasticity in Physiological Conditions and Central Nervous System Disorders
Xie, M., Wang, T., Feng, J., Ma, D., Feng, L., & Hao, Y. (2025) · Current Neuropharmacology · doi:10.2174/1570159x23666250225091729 · Cited by 7 · see citing works

Authors: Brown, G. C., & Neher, J. J.
Affiliations: University of Cambridge (GB)
German Center for Neurodegenerative Diseases (DE)
Corresponding author: Brown, Guy C.
ORCID: Brown, Guy C.
Neher, Jonas J.
Venue: Nature Reviews Neuroscience
Publisher: Springer Science and Business Media LLC
Published: 2014-03-20
Volume: 15
Issue: 4
Pages: 209-216
ISSN: 1471-003X (ISSN-L)
1471-0048
DOI: 10.1038/nrn3710
OpenAlex: W2027467386
Cited by: 853
References: 79
Citations by year: 2026: 46 · 2025: 65 · 2024: 73 · 2023: 78 · 2022: 78 · 2021: 106 · 2020: 82 · 2019: 71 · 2018: 76 · 2017: 58 · 2016: 57 · 2015: 45 · 2014: 18
FWCI: 4.72
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature reviews. Neuroscience (publishedVersion)
PubMed (publishedVersion)
DZNE Pub (submittedVersion)
Funders: Wellcome Trust (RG50995)
University of Cambridge
National Academy of Sciences of Ukraine
Medical Research Council (MR/L010593/1)
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: microglia, phagocytosis, neuronal cell death, neuronal loss, brain development, neuroinflammation, ischemia, neurodegeneration, phagocytes
MeSH terms: Animals, Humans, Neurons, Phagocytosis, Cell Death, Microglia

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Microglial Phagocytosis of Live Neurons

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