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Updated: Jun 3, 2026

Standardized Data Acquisition for Neuromelanin-Sensitive Magnetic Resonance Imaging of the Substantia Nigra
Published on: September 8, 2021
[Possible relationship of the function of dysbindin-1 with the pathophysiology of schizophrenia]
Hidenori Ito1, Koh-ichi Nagata
1Department of Molecular Neurobiology, Institute for Developmental Research, Aichi Human Service Center, 713-8 Kamiya, Kasugai, 480-0392 Japan.
Abstract:
Schizophrenia is a psychiatric disorder with a prevalence of about 1%. Genetic factors are known to be important in the etiology of schizophrenia and several susceptibility genes have been identified in linkage or association studies. Although the pathophysiology is yet to be determined, unusual neurotransmissions such as dopaminergic and glutamatergic systems have been suggested for the mechanism of schizophrenia symptoms. On the other hand, the concept that schizophrenia is a neurite malformation illness has arisen, based on the observations that DISC1 is involved in neuronal development. The gene for dysbindin-1 (DTNBP1) is situated at chromosome 6, the location of one of the most established linkages to schizophrenia. Interestingly, significant haplotypic associations between DTNBP1 and schizophrenia have been found in several studies in independent populations of schizophrenic cases. In addition, reduction of the gene and the protein of dysbindin-1 have been reported in brains from schizophrenic cases. Hence, genetic variations in DTNBP1 might be a major risk factor for schizophrenia. In the present review, we focus on the function of dysbindin-1 and its potential contributions to the pathophysiology of schizophrenia.
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