Scope

Schizophrenia is a neurodevelopmental disorder that involves a complex interplay between genetic and environmental factors that contribute to its clinical phenotype and the underlying endophenotype. Unlike the dementias, schizophrenia has no classic histopathologic features readily identifiable with standard light microscopic assessments. Rather, postmortem studies of schizophrenia reported over the past 30 years have strongly suggested that this disorder involves subtle changes in the wiring of corticolimbic circuits, particularly the dorsolateral prefrontal cortex, anterior cingulate region, hippocampus, amygdala, and basal ganglia. All of these regions play a direct and/or indirect role in the mediation of cognition and emotion. Studies from many laboratories have pointed to abnormalities associated with the GABA and glutamate systems and have provided a basis for understanding how “mis-wired” microcircuitry may provide a substrate for understanding clinical dysfunction in patients with schizophrenia. With the advent of high sensitivity, microarray-based  studies of genomic integrity, gene expression, epigenetic regulation and metabolomics, it is now possible to study neural systems in human and rodent brain and test hypotheses regarding the interaction of the glutamate and GABA systems in both health and disease. It is now evident that glutamatergic fiber systems mediated by a variety of receptor systems are capable of modulating the regulation of complex cellular and molecular pathways capable of influencing both the activity and viability of neurons located in “hot spot” regions that postmortem studies suggest are involved in the pathophysiology of schizophrenia. Abnormalities in the synaptic connectivity within regions-of-interest, such as the hippocampus, can theoretically alter the integration of neural elements found within its microcircuits and result in abnormalities in their activity and the functional output.  

As postmortem studies have suggested ways in which neural circuitry changes may contribute to abnormal integration at the micro-level, magnetic resonance (MR) and other forms of technology used to study behavior and cognition have been providing parallel and complementary views of how the metabolism of brain regions are altered and can influence the interactions within broad-based regional networks of the brain in live human subjects both with and without schizophrenia. These strategies are providing “bottom up” (cells and molecules) and “top-down”(regional activation and behavior) approaches that will eventually make it possible to generate meaningful and testable hypotheses regarding the neurobiological basis of schizophrenia.  

The Schizophrenia Section of Frontiers in Psychiatry is actively pursuing an integrative understanding of the neuroscience of schizophrenia by assembling a distinguished team of neuroscientists representing a broad range of strategies and technologies who will serve as Associate Editors.  The goal of this Section will be to provide a forum for interactions among scientists, so that an integrative approach to studies of schizophrenia will eventually achieve a comprehensive view of how cognitive and emotional behaviors altered in schizophrenia may be perturbed by changes in the cellular and molecular integrity of key brain areas involved in the mediation of cognition and emotion. 

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