The complement system: an unexpected role in synaptic pruning during development and disease.

By A. Stephan, B. Barres, Beth Stevens. Annual Review of Neuroscience, 2012

1,038 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

The Central Nervous System and the Gut Microbiome (2016, background): “Microglia produce copious amounts of C1q, the first protein in the complement activation cascade, and express various complement receptors (Schafer et al., 2012; Stephan et al., 2012).”
Microglia: Dynamic Mediators of Synapse Development and Plasticity (2015, background): “Surprisingly, classical complement proteins C1q and C3 are widely expressed in the healthy postnatal brain and localize to subsets of immature synapses [16,17], while the complement receptor 3 (CR3) is expressed in resident microglia [17,18].”
Complement and Microglia Mediate Early Synapse Loss in Alzheimer Mouse Models (2016, neutral): “Although specific receptors for C1q at synapses are not yet known, C1q binds synapses in vulnerable regions undergoing synapse loss (our data here; (5, 27)).”
iPSC-derived human microglia-like cells to study neurological diseases (2017, neutral): “Microglia along with astrocytes, also play a critical role in synaptic pruning (Aguzzi et al., 2013, Paolicelli et al., 2011, Stephan et al., 2012).”
Microglia in Alzheimer’s disease (2018, background): “During normal brain development, mounting evidence indicates that microglia engulf synapses and sculpt synaptic connections via a novel role for complement, a component of the innate immune system that enhances the clearance of microbes or damaged cells by phagocytes (Boulanger, 2009; Stephan et al.”