Role of calcium regulation in pathophysiology model of schizophrenia and possible interventions.
Recent advances into the neuroscience research related to pathophysiology of schizophrenia have been impressive. While some are based on pre-existing theories and models, others have explored on a molecular level attempting to integrate the concepts of the past and present. However, given the complex multifactorial etiology of schizophrenia attempts to improve the current treatment modalities raise more questions than answers. In the cascade model of the hypotheses, the focus will be on a common factor/marker for the disease, to address the possible stepwise correlation between the various theories. Homeostasis of calcium, its relation to the release of glutamate, dopamine and nitric oxide will be discussed in detail with the potential for interventions aimed at every stage. Although this hypothesis emphasizes the role of calcium as a common factor, other potential causes such as autoantibodies to the receptors, such as NMDA (and GABA) cannot be ruled out.
Yarlagadda
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Department of Psychiatric Medicine, University of Virginia Health System, Charlottesville, Virginia 22908-0623, USA. ary9a@virginia.edu
D001921:Brain / Q000254:growth & development / Q000503:physiopathology; D002118:Calcium / Q000378:metabolism*; D004298:Dopamine / Q000378:metabolism; D006801:Humans; D008954:Models, Biological; D009410:Nerve Degeneration / Q000503:physiopathology; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology; D012559:Schizophrenia / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy
D016194:Receptors, N-Methyl-D-Aspartate; D002118:Calcium; D004298:Dopamine