Prenatal immune activation and subsequent peripubertal stress as a new model of schizophrenia
Prenatal immune activation and subsequent peripubertal stress as a new model of schizophrenia
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DOI：
10.1586/14737175.2013.811191
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发表时间：
2013-07
影响因子：
4.3
通讯作者：
N. Yoshimi;T. Futamura;K. Hashimoto
中科院分区：
文献类型：
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作者：
N. Yoshimi;T. Futamura;K. Hashimoto
评价：Giovanoli S，Engler H，Engler A等，青春期应激揭示了小鼠产前免疫激活的潜在神经病理学后果。Science 339（6123），1095-1099（2013）.流行病学研究表明，母亲在怀孕期间的病毒感染在神经发育障碍，如精神分裂症和自闭症的病因学中起着关键作用。产前母体免疫激活和青春期心理应激是神经发育障碍的关键环境危险因素。已知病毒模拟物聚核糖肌苷-聚核糖胞苷酸作为Toll样受体-3激动剂起作用。聚核糖肌苷酸-聚核糖胞苷酸通常用于建立这种产前免疫激活的啮齿动物模型。最近，Giovanoli等人报道了一种新的精神分裂症神经发育模型，该模型基于产前免疫激活和青春期应激的结合。在本报告中，我们将这些发现置于背景中并讨论其意义。
Evaluation of: Giovanoli S, Engler H, Engler A et al. Stress in puberty unmasks latent neuropathological consequences of prenatal immune activation in mice. Science 339(6123), 1095–1099 (2013). Epidemiological studies show that maternal viral infection during pregnancy plays a key role in the etiology of neurodevelopmental disorders, such as schizophrenia and autism. Prenatal maternal immune activation and peripubertal psychological stress are key environmental risk factors for neurodevelopmental disorders. Viral mimic polyriboinosinic-polyribocytidylic acid is known to act as a Toll-like receptor-3 agonist. Polyriboinosinic-polyribocytidylic acid has been typically used to establish this rodent model of prenatal immune activation. Recently, Giovanoli et al. reported on a new neurodevelopmental model of schizophrenia based on combined prenatal immune activation and peripubertal stress. In this report, we place these findings into context and discuss their significance.