Cited by 32Neuroinflammation and Neurodegeneration MechanismsNeuroscience and Neuropharmacology ResearchNeurogenesis and neuroplasticity mechanisms

Loss of microglial EED impairs synapse density, learning, and memory

Wang, Ying-Ying, Deng, Yu-Sen, Dai, Shang-Kun, Mi, Ting-Wei, Li, Rui-Yang, Liu, Pei-Pei, Liu, Cong, He, Bao-Dong +6 more·2022·Molecular Psychiatry

Abstract

The embryonic ectoderm development (EED) is a core component of the polycomb-repressive complex 2 (PRC2) whose mutations are linked to neurodevelopmental abnormalities, intellectual disability, and neurodegeneration. Although EED has been extensively studied in neural stem cells and oligodendrocytes, its role in microglia is incompletely understood. Here, we show that microglial EED is essential for synaptic pruning during the postnatal stage of brain development. The absence of microglial EED at early postnatal stages resulted in reduced spines and impaired synapse density in the hippocampus at adulthood, accompanied by upregulated expression of phagocytosis-related genes in microglia. As a result, deletion of microglial Eed impaired hippocampus-dependent learning and memory in mice. These results suggest that microglial EED is critical for normal synaptic and cognitive functions during postnatal development.

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Crossref · 10.1038/s41380-022-01576-w

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  • The EED gene codes for a core component of the polycomb-repressive complex 2, which has been linked to neurodevelopmental abnormalities, intellectual disability, and neurodegeneration, and microglial EED has been suggested to play a pivotal role in normal synaptic and cognitive functions.

    “The embryonic ectoderm development gene (EED) codes for a core component of the polycomb-repressive complex 2, which has been linked to neurodevelopmental abnormalities, intellectual disability, and neurodegeneration, and microglial EED has been suggested to play a pivotal role in normal synaptic and cognitive functions (Wang et al., 2022).”

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Authors
Wang, Y.-Y., Deng, Y.-S., Dai, S.-K., Mi, T.-W., Li, R.-Y., Liu, P.-P., Liu, C., He, B.-D., He, X.-C., Du, H.-Z., Yang, H.-C., Tang, Y., Liu, C.-M., & Teng, Z.-Q.
Affiliations
  • Chinese Academy of Sciences (CN)
  • Capital Medical University (CN)
Corresponding author
  • Liu, Cong
  • Tang, Yi
  • Liu, Chang-Mei
  • Teng, Zhao-Qian
Venue
Molecular Psychiatry
Published
2022-04-28
Volume
27
Issue
7
Pages
2999-3009
ISSN
  • 1359-4184 (ISSN-L)
  • 1476-5578
OpenAlex
W4225015717
Cited by
32
References
62
Citations by year
2026: 4 · 2025: 6 · 2024: 9 · 2023: 10 · 2022: 3
FWCI
2.46
Type
journal article
Language
en
Open access
closed
Locations
  • Molecular Psychiatry (publishedVersion)
  • PubMed (publishedVersion)
Funders
the National Key Research and Development Program of China Project
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Keywords
EED, microglia, polycomb repressive complex 2, synaptic pruning, synaptic density, dendritic spines, hippocampus, learning and memory, phagocytosis, postnatal brain development, intellectual disability, neurodevelopmental disorders
MeSH terms
Animals, Hippocampus, Synapses, Microglia, Mice, Neural Stem Cells, Polycomb Repressive Complex 2

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