Development of a new therapeutic target molecule for schizophrenia from antipsychotics signaling

我们已经确定了两个分子作为Fyn介导的抗精神病信号的下游底物。对于其中一个分子，我们还确定了抗精神病药物介导的磷酸化位点。使用死后大脑样本，我们发现与对照组相比，精神分裂症患者额叶皮质中Fyn蛋白水平增加。此外，在精神分裂症患者的大脑中，参与单胺胞吐的CADPS2的mRNA表达增加。精神分裂症患者脑脊液中Fyn上游调节因子IL-6和多巴胺代谢产物HVA水平升高。因此，我们已经确定了一组参与抗精神病信号的分子，并发现这些分子中的一部分应该参与精神分裂症的病理。这些分子是否可能成为精神分裂症的治疗靶点，还需要进一步的研究来澄清。

We have identified two molecules as downstream substrates for Fyn-mediate anti-psychotic signaling. For one of those molecules, we also determined antipsychotics-mediate phosphorylation sites. Using post-mortem brain samples, we found that the Fyn protein levels are increased in the schizophrenia frontal cortices compared to the controls. Also, the mRNA expression of CADPS2, which is involved in the exocytosis of monoamines, was increased in schizophrenia brains. In the cerebrospinal fluids, the levels of IL-6, which is upstream regulator of Fyn, and the levels of dopamine metabolite, HVA, were increased in schizophrenia. Thus, we have identified a group of molecules involved in antipsychotic signaling and, found that a part of those molecules should be involved in the schizophrenia pathology. Further research is required to clarify whether those molecules could be therapeutic targets for schizophrenia.