Complement-dependent synaptic elimination during development and disease

Abstract summary

Reviewed evidence that the complement cascade, including C1q and C3, tags synapses for elimination by microglia throughout development and in disease. Highlighted how this mechanism becomes aberrantly reactivated in aging and neurodegeneration. Microglia express complement receptors (including CR3/ITGAM) to mediate synaptic pruning.

Evidence labels

Therapeutic relevance

Complement-mediated synapse elimination identified as targetable mechanism in neurodegeneration; C1q, C3, and CR3 are therapeutic targets.