Microglial Over-Pruning of Synapses During Development in Autism-Associated SCN2A-Deficient Mice and Human Cerebral Organoids

Scientists established a microglia-incorporated human cerebral organoid model carrying an SCN2A protein-truncating mutation identified in children with autism spectrum disorder. They found that human microglia display increased elimination of post-synapse in cerebral organoids carrying the SCN2A mutation.