Local apoptotic-like mechanisms underlie complement-mediated synaptic pruning

• DOI: 10.1073/pnas.1722613115
• Publication Date: 2018-05-29T15:39:45Z
• Authors: Balázs A. Györffy; Judit Kun; György Török; Éva Bulyáki; Zsolt Borhegyi; Péter Gulyássy; Viktor Kis; Péter Szocsics; András Micsonai; János Matkó; László Drahos; Gábor Juhász; Katalin A. Kékesi; József Kardos
• Keywords: Male; Proteomics; 0301 basic medicine; Neuronal Plasticity; Proteome; Complement C1q; Apoptosis; Neurodegenerative Diseases; Biological Sciences; 03 medical and health sciences; Phagocytosis; Synapses; Humans; Microglia; Complement Activation; QR180 Immunology / immunológia; Aged

Significance Synaptic pruning is dominant in early ontogenesis when a large number of unnecessary synapses are eliminated, and it maintains synaptic plasticity in the mature healthy brain, e.g., in memory processes. Its malfunction is involved in degenerative diseases such as Alzheimer’s disease. C1q, a member of the immune complement system, plays a central role in the selective pruning of synapses by microglial phagocytosis. Understanding the molecular aspects of complement-mediated synapse elimination is of high importance for developing effective therapeutic interventions in the future. Our analysis on C1q-tagged synaptosomes revealed that C1q label-based synaptic pruning is linked to local apoptotic-like processes in synapses.