Elevated Prenatal Homocysteine Levels as a Risk Factor for Schizophrenia

Abstract
Compelling evidence suggests that a disruption of neurodevelopment during fetal life plays a role in the etiology of schizophrenia.1,2 Risk factors that are known to produce neurodevelopmental insult and that have been implicated in schizophrenia include prenatal viral infection,3,4 prenatal nutritional deficiency,5 fetal hypoxia,6 and perinatal insults.2 Despite significant advances, these and other prenatal exposures have not been definitively linked with neurochemical perturbations proposed in this illness. The identification of such a risk factor could help to unify current hypotheses on neurodevelopmental mechanisms and neurotransmitter function in schizophrenia.

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