Laboratory of Behavioural Neurobiology, Swiss Federal Institute of Technology (ETH) Zurich, 8603 Schwerzenbach, Switzerland.
Pediatr Res. 2011 May;69(5 Pt 2):26R-33R. doi: 10.1203/PDR.0b013e318212c196.
Prenatal exposure to infection and subsequent inflammatory responses have been implicated in the etiology of schizophrenia and autism. In this review, we summarize current evidence from human and animal studies supporting the hypothesis that the pathogenesis of these two disorders is linked via exposure to inflammation at early stages of development. Moreover, we propose a hypothetical model in which inflammatory mechanisms may account for multiple shared and disorder-specific pathological characteristics of both entities. In essence, our model suggests that acute neuroinflammation during early fetal development may be relevant for the induction of psychopathological and neuropathological features shared by schizophrenia and autism, whereas postacute latent and persistent inflammation may contribute to schizophrenia- and autism-specific phenotypes, respectively.
产前感染和随后的炎症反应与精神分裂症和自闭症的病因有关。在这篇综述中，我们总结了来自人类和动物研究的现有证据，支持这样一种假设，即这两种疾病的发病机制通过在发育早期暴露于炎症而联系在一起。此外，我们提出了一个假设模型，其中炎症机制可能解释了这两种疾病的多个共同和特定于疾病的病理特征。从本质上讲，我们的模型表明，早期胎儿发育期间的急性神经炎症可能与精神分裂症和自闭症共有的精神病理学和神经病理学特征的诱导有关，而急性后潜伏和持续的炎症可能分别导致精神分裂症和自闭症的特异性表型。
