Development ofa new therapy by a risk gene for schizophrenia

在精神分裂症的脑组织中观察到精神分裂症的危险基因dysbindin的表达水平降低，并且在dysbindin缺陷小鼠中发现类似于精神分裂症患者的行为异常。在过量表达dysbindin蛋白的dysbindin转基因小鼠中，当PCP引起类似精神分裂症的阳性和阴性症状时，我们发现过量表达dysbindin蛋白可以保护PCP引起的一些行为异常。由于在dysbindin转基因小鼠中发现了包括EGFR 2在内的转录因子的基因表达的变化，因此提出了通过转录因子的dysbindin信号通路参与保护作用的可能性。

The reduced expression level of dysbindin, which is a risk gene of schizophrenia, was observed in schizophrenia brain and the behavioral abnormalities similar to patients with schizophrenia were found in dysbindin deficient mouse. When PCP which causes the positive and negative sympotoms similar to schizophrenia were treated in dysbindin transgenic mouse overexpressing dysbindin protein, we found overexpression of dysbindin protein protected some behavioral abnormalities induced by PCP. Since change of the gene expression of transcription factors including EGR2 was found in dysbindin transgenic mouse, a possibility that the dysbindin signaling pathway through a transcription factor was participating in the protective action was suggested.