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Animal models may help fractionate shared and discrete pathways underpinning schizophrenia and autism

机译:动物模型可能有助于分离支持精神分裂症和自闭症的共享和离散途径

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Crespi & Badcock (C&B) present an appealing and parsimonious synthesis arguing that schizophrenia and autism are differentially regulated by maternal versus paternal genomie imprinting, respectively. We argue that animal models related to schizophrenia and autism provide a useful platform to explore the mechanisms outlined by C&B. We also note that schizophrenia and autism share certain risk factors such as advanced paternal age. Apart from genomie imprinting, copy number variants related to advanced paternal age may also contribute to the differential trajectory of brain development associated with autism and schizophrenia.
机译:Crespi&Badcock(C&B)提出了一种吸引人的和简约的综合方法,认为精神分裂症和自闭症分别受母体和父体基因组印记的差异调节。我们认为与精神分裂症和自闭症有关的动物模型为探讨C&B概述的机制提供了一个有用的平台。我们还注意到,精神分裂症和自闭症具有某些危险因素,例如父辈高龄。除了基因组印记外,与父辈高龄有关的拷贝数变异也可能导致与自闭症和精神分裂症相关的大脑发育的不同轨迹。

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