Abstract
Despite recent advances in neuroscience, fundamental cause of schizophrenia still remains unknown and, thus far, our only effective antipsychotic drugs (dopamine antagonists) that rarely reach to complete remission are still based on the classical dopamine hypothesis. Thus, we need a novel hypothesis and translatable biomarker that enables early diagnosis, intervention and complete remission. Recent evidences show that abnormality in gamma-band (30-100 Hz) oscillations which relates to perception and cognition, exhibit neuronal deficits in schizophrenia. Impairments in gamma-band oscillation have been hypothesized to cause from disruptions of GABAergic inhibitory interneuron one act as a pacemaker in neural circuit, and excitatory neuron (NMDAR hypofunction) , as well as aberrant neuronal balance of excitation and inhibition (E/I balance) or disruptions in these tunings. Moreover, gamma-band oscillation deficit has attracted a lot of attention as a new pathophysiological model of schizophrenia and its therapeutic target since these phenomena can be obtained from animal models of schizophrenia. This presentation will review recent findings of gamma-band oscillation deficits in schizophrenia and illustrate its clinical usefulness as a novel translatable biomarker that give rise to critical features of neural dysfunction associated with schizophrenia.
