ArticleJournal of neuroinflammation2024
Microglia mediate memory dysfunction via excitatory synaptic elimination in a fracture surgery mouse model.
Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Sedanolide alleviates LPS‑induced depressive‑like behaviors by modulating the C3a/C3aR signaling axis and microglial glycolysis.Molecular medicine reports · 2026Article
- Sleep Deprivation and Neuronal Hyperexcitation Share Transcriptomic Signatures.Neuropsychopharmacology reports · 2026Article
- Microglial galectin-3 disrupts parvalbumin interneurons and hippocampal synchrony, driving cognitive deficits.Journal of neuroinflammation · 2026Article
- Microglial Ccl4-Ccr5 signaling links systemic inflammation to synaptic loss and memory deficits in chronic kidney disease.Journal of neuroinflammation · 2026Article
- LCN2/SLC22A17 mediates the phagocytosis of GABAergic synapses by oligodendrocyte progenitor cells and contributes to cancer-induced pain and comorbid anxiety-like behaviors in mice.Acta neuropathologica communications · 2026Article
- Astrocytic EAAT1 suppression by EV-ACLY underlies glutamate imbalance and cognitive impairment in POCD.Communications biology · 2026Article
- Ozone-induced cognitive deficits are mediated by the liver-brain axis: peripheral complement C3 triggers microglial synaptic phagocytosis.Journal of neuroinflammation · 2026Article
- Microglial pathological synaptic pruning in epilepsy: pathophysiology and therapeutic potential.Frontiers in immunology · 2026Review
- Perioperative neurocognitive disorders as a neuroimmune landscape disorder: microglial priming, state heterogeneity, and time-dependent neuroinflammation.Frontiers in immunology · 2026Review
- Microglial PGC-1α alleviates synaptic damage and cognitive impairments following anesthesia and surgery by suppressing excessive synaptic pruning in aged mice.International journal of biological sciences · 2026Article
- RNA-binding protein RBM47 in health and disease: molecular mechanisms, preclinical evidence, and translational challenges.Frontiers in immunology · 2026Review
- Microglial RUNX1/RBM47 ablation inhibits neuronal ferroptosis via regulating the cGAS-STING-MEF2C pathway in mice with postoperative cognitive dysfunction.Communications biology · 2025Article
- Transglutaminase-2 Promotes Microglial Synaptic Phagocytosis and Ameliorates Epileptic Seizures by Inhibiting ABCA1 Ubiquitination.CNS neuroscience & therapeutics · 2025Article
- Opposing roles of microglial and macrophagic C3ar1 signaling in stress-induced synaptic and behavioral changes.Molecular psychiatry · 2025Article
- Article
- Senescent Microglia Mediate Neuroinflammation-Induced Cognitive Dysfunction by Selective Elimination of Excitatory Synapses in the Hippocampal CA1.Aging cell · 2025Article
- P2X7-CaMKII drives 5-LOX nuclear translocation to impair microglial function after subarachnoid hemorrhage.Journal of neuroinflammation · 2025Article
- Photo-Biomodulation of the Hippocampus Using Near-Infrared Laser to Enhance Cognitive Function in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Reduced synaptic tagging by complement protein C3 is associated with elevated extracellular matrix in the middle-aged cerebellum of mice.Frontiers in aging neuroscience · 2025Article
- Targeting complement C3 with Tanshinone I decreases microglia-mediated synaptic engulfment to exert antidepressant effects.Theranostics · 2025Article
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Authors and funding
11 authors.
Funding
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Abstract
Cognitive impairment is a common issue among human patients undergoing surgery, yet the neural mechanism causing this impairment remains unidentified. Surgical procedures often lead to glial cell activation and neuronal hypoexcitability, both of which are known to contribute to postoperative cognitive dysfunction (POCD). However, the role of neuron-glia crosstalk in the pathology of POCD is still unclear. Through integrated transcriptomics and proteomics analyses, we found that the complement cascades and microglial phagocytotic signaling pathways are activated in a mouse model of POCD. Following surgery, there is a significant increase in the presence of complement C3, but not C1q, in conjunction with presynaptic elements. This triggers a reduction in excitatory synapses, a decline in excitatory synaptic transmission, and subsequent memory deficits in the mouse model. By genetically knockout out C3ar1 or inhibiting p-STAT3 signaling, we successfully prevented neuronal hypoexcitability and alleviated cognitive impairment in the mouse model. Therefore, targeting the C3aR and downstream p-STAT3 signaling pathways could serve as potential therapeutic approaches for mitigating POCD.
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