A variety of functional MRI (fMRI) studies revealed disturbed connectivity in complex hippoampal, prefrontal and cerebellar-thalamic-prefrontal networks in schizophrenia [31]. In patients and non-psychotic subjects at increased risk dynamic causal modeling in fMRI studies revealed decreased effective connectivity between the posterior hippocampus and prefrontal cortex during working memory tasks [3, 23]. According to these results, postmortem studies revealed a loss of myelin-building oligodendrocytes in prefrontal and hippocampal subregions, leading to impaired nerve cell propagation of information [24, 36]. Furthermore, gene expression of oligodendrocyte-related genes is decreased in schizophrenia. An additional synaptopathy with decreased expression of glutamatergic and gamma-amino-butyric acid (GABA)ergic synaptic proteins and consecutive disturbance of microconnectivity [7, 25] is completing the complex framework of disconnectivity in schizophrenia.
