A large body of neuroimaging literature suggests that distributed regions in the brain form coordinated largescale
networks that show reliable patterns of connectivity when observed using either functional or structural magnetic
resonance imaging (MRI) methods. Functional activation within these networks provides a robust and reliable representation
of dynamic brain states observed during information processing. One such network comprised of anterior frontoinsular
cortex (aFI) and anterior cingulate cortex (ACC) is called the Salience Network (SN). SN has been identified as a
system that enables the switch between various dynamic brain states. SN dysfunction has been proposed as a mechanistic
model for several core symptoms of schizophrenia. In this review, we explore how various risk factors of schizophrenia
could operate through the dysfunctional SN to generate symptoms of psychosis. We also consider the putative neurochemical
basis for the SN dysfunction in schizophrenia, and suggest that the SN dysfunction is a viable therapeutic target
for a combined pharmacological and cognitive training treatment approach. This combination approach, termed as Brain
Network Modulation, could exploit neuronal plasticity to reverse a key pathophysiological deficit in schizophrenia.
Keywords: Anterior cingulate, Brain Network Modulation, Dopamine, Glutamate, Insula, Plasticity, Salience network, Schizophrenia.
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