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Review
. 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?

Urs Meyer  1 , Joram Feldon, Olaf Dammann
Affiliations
Review

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

Urs Meyer et al. Pediatr Res. 2011 May.

Abstract

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.

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Figures

Figure 1
Figure 1. A model of inflammation leading to both shared and disorder-specific features of schizophrenia and autism
Maternal infection during critical stages of pregnancy leads to acute fetal inflammation. The consequences of acute fetal neuroinflammation on early neurodevelopmental consequences may facilitate the development of psychopathological and neuropathological phenotypes shared between schizophrenia and autism. Upon the initiation of acute fetal inflammation, the maternal and/or fetal system may then either be driven into persistent inflammation, or alternatively may gain control over the ongoing inflammatory process. The genetic background may critically influence the transition of acute fetal inflammation into either persistence or suppression of inflammation. The occurrence of persistent inflammation may be related to a failure in the negative feedback control of inflammation, and may eventually result in chronic inflammation persisting into the perinatal period and beyond. By contrast, mounting sufficient anti-inflammatory and/or immunosuppressive activity in the maternal and/or fetal systems may counteract the acute fetal inflammatory response on the one hand, but on the other hand, may prime the early life organisms to latent immune abnormalities persisting into the postnatal period. Latent inflammation may then be unmasked in postnatal life by exposure to specific environmental stimuli such as stress or immune re-exposure. Persistent inflammation may be more relevant for the etiopathogenesis of autism, and thus may contribute to phenotypic abnormalities specifically seen in autism. On the other hand, latent immune abnormalities may be essential to the pathogenesis of schizophrenia-specific brain abnormalities. The genetic background further contributes to the emergence of unique brain dysfunctions independently of or in interaction with the outlined inflammatory pathways.
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