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- W2806131738 abstract "C1q, a member of the immune complement cascade, is implicated in the selective pruning of synapses by microglial phagocytosis. C1q-mediated synapse elimination has been shown to occur during brain development, while increased activation and complement-dependent synapse loss is observed in neurodegenerative diseases. However, the molecular mechanisms underlying C1q-controlled synaptic pruning are mostly unknown. This study addresses distortions in the synaptic proteome leading to C1q-tagged synapses. Our data demonstrated the preferential localization of C1q to the presynapse. Proteomic investigation and pathway analysis of C1q-tagged synaptosomes revealed the presence of apoptotic-like processes in C1q-tagged synapses, which was confirmed experimentally with apoptosis markers. Moreover, the induction of synaptic apoptotic-like mechanisms in a model of sensory deprivation-induced synaptic depression led to elevated C1q levels. Our results unveiled that C1q label-based synaptic pruning is triggered by and directly linked to apoptotic-like processes in the synaptic compartment." @default.
- W2806131738 created "2018-06-13" @default.
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- W2806131738 date "2018-05-29" @default.
- W2806131738 modified "2023-10-18" @default.
- W2806131738 title "Local apoptotic-like mechanisms underlie complement-mediated synaptic pruning" @default.
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- W2806131738 doi "https://doi.org/10.1073/pnas.1722613115" @default.
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