A growing body of evidence suggests that immune alterations, especially those related
to inflammation, are associated with increased risk of schizophrenia and schizophrenia-related
brain alterations. Much of this work has focused on the prenatal period, because infections
during pregnancy have been repeatedly (albeit inconsistently) linked to risk of schizophrenia.
Given that most infections do not cross the placenta, cytokines associated with inflammation
(proinflammatory cytokines) have been targeted as potential mediators of the damaging
effects of infection on the fetal brain in prenatal studies. Moreover, additional
evidence from both human and animal studies suggests links between increased levels
of proinflammatory cytokines, immune-related genes, and schizophrenia as well as brain
alterations associated with the disorder. Additional support for the role of altered
immune factors in the etiology of schizophrenia comes from neuroimaging studies, which
have linked proinflammatory cytokine gene polymorphisms with some of the structural
and functional abnormalities repeatedly found in schizophrenia. These findings are
reviewed and discussed with a life course perspective, examining the contribution
of inflammation from the fetal period to disorder presentation. Unexplored areas and
future directions, such as the interplay between inflammation, genes, and individual-level
environmental factors (e.g., stress, sleep, and nutrition), are also discussed.
Key Words
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Article info
Publication history
Published online: February 14, 2013
Accepted:
January 2,
2013
Received in revised form:
December 7,
2012
Received:
June 14,
2012
Identification
Copyright
© 2013 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.