C1q-mediated synapse loss by microglial phagocytosis is associated with postoperative neurocognitive disorder in mice
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The authors investigate the role of complement C1q in microglial activation and synapse loss as potential mechanisms contributing to postoperative neurocognitive disorders (PNDs) in mice. Their findings indicate that increased C1q levels lead to microglial phagocytosis of synapses, resulting in cognitive deficits following surgery, and suggest that targeting C1q and NF-κB activation may offer therapeutic strategies to mitigate PNDs.
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