The PI3K signaling pathway as a pharmacological target in Autism related disorders and Schizophrenia.

Molecular and cellular therapies Pub Date : 2016-02-11 eCollection Date: 2016-01-01
Lilian Enriquez-Barreto, Miguel Morales
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引用次数: 0

Abstract

This review is focused in PI3K's involvement in two widespread mental disorders: Autism and Schizophrenia. A large body of evidence points to synaptic dysfunction as a cause of these diseases, either during the initial phases of brain synaptic circuit's development or later modulating synaptic function and plasticity. Autism related disorders and Schizophrenia are complex genetic conditions in which the identification of gene markers has proved difficult, although the existence of single-gene mutations with a high prevalence in both diseases offers insight into the role of the PI3K signaling pathway. In the brain, components of the PI3K pathway regulate synaptic formation and plasticity; thus, disruption of this pathway leads to synapse dysfunction and pathological behaviors. Here, we recapitulate recent evidences that demonstrate the imbalance of several PI3K elements as leading causes of Autism and Schizophrenia, together with the plausible new pharmacological paths targeting this signaling pathway.

PI3K信号通路作为自闭症相关障碍和精神分裂症的药理靶点。
本综述的重点是PI3K在两种广泛存在的精神疾病:自闭症和精神分裂症中的作用。大量证据表明突触功能障碍是导致这些疾病的原因,要么是在大脑突触回路发育的初始阶段,要么是后来调节突触功能和可塑性的阶段。自闭症相关疾病和精神分裂症是复杂的遗传疾病,尽管在这两种疾病中存在高患病率的单基因突变,为了解PI3K信号通路的作用提供了见解,但事实证明,鉴定基因标记是困难的。在大脑中,PI3K通路的组分调节突触的形成和可塑性;因此,该通路的破坏导致突触功能障碍和病理行为。在这里,我们总结了最近的证据,证明几个PI3K元素的不平衡是自闭症和精神分裂症的主要原因,以及针对这一信号通路的合理的新药理学途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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