Schizophrenia and autism: both shared and disorder-specific pathogenesis via perinatal inflammation?
Schizophrenia and autism: both shared and disorder-specific pathogenesis via perinatal inflammation?
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DOI：
10.1203/pdr.0b013e318212c196
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发表时间：
2011-05
影响因子：
3.6
通讯作者：
Dammann O
中科院分区：
文献类型：
--
作者：
Meyer U;Feldon J;Dammann O
产前接触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当前证据，支持以下假设：这两种疾病的发病机制与发育早期阶段的炎症暴露有关。此外，我们提出了一个假设模型，其中炎症机制可能解释两个实体的多种共享和疾病特异性病理特征。从本质上讲，我们的模型表明，胎儿早期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，而急性后潜伏性和持续性炎症可能分别导致精神分裂症和自闭症特异性表型。
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, while post-acute latent and persistent inflammation may contribute to schizophrenia- and autism-specific phenotypes, respectively.