Frontal Cortical Networks, Impaired Cognitive Control and Disorganization in Schizophrenia

Abstract

Event Abstract Back to Event Frontal Cortical Networks, Impaired Cognitive Control and Disorganization in Schizophrenia Cameron Carter1* 1 University of California, Davis, United States Schizophrenia is a common mental disorder affecting both genders and at least 1% of the population. It has its onset in late adolescence and leads to major personal and family disruption and for many individuals lifelong impairment in social and social functioning. Impaired cognition in schizophrenia is present at the onset of the illness, persists across the lifespan and is the strongest predictor of poor functional outcome in the illness. Our presently available treatments have little if any impact on this aspect of the illness making developing effective treatments for impaired cognition in schizophrenia a critical challenge for biomedicine in the 21st century. People with schizophrenia are impaired across a range of cognitive functions including attention, working and episodic memory and language comprehension and production. One parsimonious theory that draws upon an influential model from cognitive neuroscience is that patents have impairments of cognitive control, in the service of which the prefrontal cortex supports task appropriate performance by recruiting task appropriate networks across the brain. fMRI studies support the presence of PFC dysfunction in schizophrenia that is associated with impaired recruitment of task appropriate networks and these deficits are independent of medication status or stage of the illness. They also predict the level of clinical disorganization in patients as well as their level of functioning. Post mortem studies in schizophrenia suggest altered connectivity in local circuits in the prefrontal cortex that participate in the establishment of high frequency (gamma band) oscillations. Furthermore cognitive EEG studies in schizophrenia show reduced cognitive control related gamma oscillations across frontal electrodes in schizophrenia. These suggest a model of schizophrenia in which altered development of local networks impair the ability to endogenously generate gamma synchrony in the PFC, and this leads to altered recruitment of task appropriate networks, cognitive impairment, behavioral disorganization and impaired functioning. Recent refinements in the cognitive control model of cognitive impairment in schizophrenia will be discussed in addition to strategies for developing effective treatments for impaired cognition in the illness.