Send to

Choose Destination
Pediatr Res. 2011 May;69(5 Pt 2):26R-33R. doi: 10.1203/PDR.0b013e318212c196.

Schizophrenia and autism: both shared and disorder-specific pathogenesis via perinatal inflammation?

Author information

Laboratory of Behavioural Neurobiology, Swiss Federal Institute of Technology (ETH) Zurich, 8603 Schwerzenbach, Switzerland.


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.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center