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Prenatal immune activation and subsequent peripubertal stress as a new model of schizophrenia

Evaluation of: Giovanoli S, Engler H, Engler A et al. Stress in puberty unmasks latent neuropathological consequences of prenatal immune activation in mice. Science 339(6123), 1095–1099 (2013). Epidemiological studies show that maternal viral infection during pregnancy plays a key role in the etiology of neurodevelopmental disorders, such as schizophrenia and autism. Prenatal maternal immune activation and peripubertal psychological stress are key environmental risk factors for neurodevelopmental disorders. Viral mimic polyriboinosinic-polyribocytidylic acid is known to act as a Toll-like receptor-3 agonist. Polyriboinosinic-polyribocytidylic acid has been typically used to establish this rodent model of prenatal immune activation. Recently, Giovanoli et al. reported on a new neurodevelopmental model of schizophrenia based on combined prenatal immune activation and peripubertal stress. In this report, we place these findings into context and discuss their significance.