A confluence of evidence supports an association between prenatal inflammation and risk of schizophrenia. Outside of studies of prenatal infections and risk of schizophrenia, other relevant human studies of prenatal inflammation and neurodevelopment in schizophrenia have not been reviewed. In this paper, we review human studies of 1) prenatal inflammation and risk of schizophrenia, 2) inflammation as a potential common mediator of several prenatal risk factors for schizophrenia other than prenatal infections, 3) prenatal inflammation and immune function, neurocognition, brain morphology, and gene expression in adult offspring with schizophrenia, and 4) gene by environment and gene by gene interactions relevant to these associations. We suggest future areas for human studies research based on existing findings.
|Original language||English (US)|
|Number of pages||9|
|Journal||Progress in Neuro-Psychopharmacology and Biological Psychiatry|
|State||Published - Apr 5 2013|
ASJC Scopus subject areas
- Biological Psychiatry