| Literature DB >> 35484239 |
Ying-Ying Wang1,2,3,4, Yu-Sen Deng1,2,3, Shang-Kun Dai1,2,3, Ting-Wei Mi1, Rui-Yang Li5, Pei-Pei Liu1,3,4, Cong Liu1,3,4, Bao-Dong He1,2,3, Xuan-Cheng He1,3,4, Hong-Zhen Du1,3,4, Han-Chen Yang5, Yi Tang6, Chang-Mei Liu7,8,9,10, Zhao-Qian Teng11,12,13,14.
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.Entities:
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Year: 2022 PMID： 35484239 DOI： 10.1038/s41380-022-01576-w
Source DB: PubMed Journal: Mol Psychiatry ISSN： 1359-4184 Impact factor: 15.992