Similarly, anomalous synaptic deficits are postulated to be important components of pathology associated with schizophrenia, as reduced dendritic spine densities [332–334] and disrupted PNNs in similar cortical regions (e.g., layer 3 of the prefrontal cortex [195]) have been reported, in addition to aberrant microglial elimination of synapses in schizophrenia patient-derived neural cultures [335] that is related in part to disease variants in complement component 4 (C4) [335, 336]. This evidence concerns the gene C4A and schizophrenia.