Schizophrenia is a severe neurodevelopmental disorder with genetic and environmental etiologies. Prenatal viral/bacterial infections and inflammation play major roles in the genesis of schizophrenia. In this review, we describe a viral model of schizophrenia tested in mice whereby the offspring of mice prenatally infected with influenza at E7, E9, E16, and E18 show significant gene, protein, and brain structural abnormalities postnatally. Similarly, we describe data on rodents exposed to bacterial infection or injected with a synthetic viral mimic (PolyI:C) also demonstrating brain structural and behavioral abnormalities. Moreover, human serologic data has been indispensible in supporting the viral theory of schizophrenia. Individuals born seropositive for bacterial and viral agents are at a significantly elevated risk of developing schizophrenia. While the specific mechanisms of prenatal viral/bacterial infections and brain disorder are unclear, recent findings suggest that the maternal inflammatory response may be associated with fetal brain injury. Preventive and therapeutic treatment options are also proposed. This review presents data related to epidemiology, human serology, and experimental animal models which support the viral model of schizophrenia.
|Original language||English (US)|
|Number of pages||14|
|Journal||Progress in Neuro-Psychopharmacology and Biological Psychiatry|
|State||Published - Apr 5 2013|
Bibliographical noteFunding Information:
We would like to thank Tim Folsom for the critical review of this manuscript. The work of S.H. Fatemi was supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development grants 5R01HD046589-04 , 3R01HD046589-04S1 , and Young & the Phyllis and Perry Schwartz Established Investigator Awards from NARSAD .
- Viral infection