Article

Prenatal infectious and nutritional factors and risk of adult schizophrenia

New York State Psychiatric Institute, 1051 Riverside Drive, Unit 23, New York, NY 10032, USA.
Expert Review of Neurotherapeutics (Impact Factor: 2.83). 08/2007; 7(7):797-805. DOI: 10.1586/14737175.7.7.797
Source: PubMed

ABSTRACT Schizophrenia is a severely disabling psychiatric disorder. Despite a considerable amount of research on the underpinnings of the disorder, its etiology and pathogenesis remain unknown. In utero exposures, including infection and nutritional deficiencies, are emerging important risk factors for schizophrenia, in which neurodevelopmental influences probably play an important role. Our group and others have embarked on investigations aimed at identifying these risk factors and examining the mechanisms by which they increase vulnerability to this disorder. This work has the potential to lead to strategies aimed at preventing this disorder and to reveal new molecular targets for pharmacotherapeutic intervention.

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    • "doi:10.1016/j.bbr.2008.12.016 The association of schizophrenia with maternal infection is not specific to influenza, however, as there is similar serological evidence linking maternal rubella, toxoplasma and genital/ reproductive infections with schizophrenia [14] [19]. Moreover, new findings have revealed an association between elevated risk for schizophrenia and maternal bacterial infection [20]. "
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    ABSTRACT: There is increasing evidence of immune involvement in both schizophrenia and autism. Of particular interest are striking abnormalities in the expression of immune-related molecules such as cytokines in the brain and cerebral spinal fluid (CSF). It is proposed that this represents a permanent state of brain immune dysregulation, which begins during early development. One possibility is that maternal infection, a known risk factor for schizophrenia and autism, sets this immune activation in motion. Several animal models are being used to investigate this hypothesis. There is also recent evidence that, among schizophrenic subjects, those associated with maternal infection display a distinctive pathology, which suggests that diverse causes for this disorder may explain some of its heterogeneity. The human and animal results related to immune involvement suggest novel therapeutic avenues based on immune interventions.
    Behavioural brain research 12/2009; 204(2):313-21. DOI:10.1016/j.bbr.2008.12.016 · 3.39 Impact Factor
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    • "Extreme natural experiments such as the Chinese and Dutch famines have provided evidence in support of this theory. Poor foetal nutrition impacts on brain development and the risk of neuropsychiatric disease is also increased (Altschuler, 2005; Kyle & Pitcherd, 2006; Penner & Brown, 2007). Moreover, maternal poor nutrition and in particular protein restriction affects the hypothalamic–pituitary– adrenal (HPA) axis, by decreasing placental 11b- hydroxysteroid dehydrogenase (11b-HSD) functioning (Seckl & Holmes, 2007). "
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    ABSTRACT: The aim of this paper was to review the literature on the biological effects of a maternal eating disorder (ED) (and relevant comorbidities) in pregnancy on mothers and in particular on the foetus. We also aimed to highlight possible mechanisms of risk for long-term consequences in the offspring. Relevant literature was searched for using PubMed, PsychInfo and Google Scholar and manually through relevant research papers. The consequences of maternal EDs in pregnancy on EDs symptoms, psychopathology and perinatal outcomes are discussed. A developmental model of possible risk mechanisms for adverse long-term nutritional and psychopathological outcomes in the offspring is proposed. Maternal EDs during pregnancy are likely to have important long-term biological effects on the foetus. Further research needs to clarify potential biological risk mechanisms highlighted in this review.
    European Eating Disorders Review 11/2009; 17(6):448-54. DOI:10.1002/erv.963 · 1.38 Impact Factor
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    • "There is an increasing body of evidence suggesting that events occurring within the intrauterine or perinatal environment can produce subtle structural injury and neurochemical deficits that result in behavioural dysfunction only after adolescence. These early disturbances are increasingly thought to play a role in the aetiology of schizophrenia [35] [45]. One of the most persuasive theories is the notion that exposure to infection in utero might contribute to the risk of later development of psychosis [11]. "
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    ABSTRACT: Early exposure to infection is known to affect brain development and has been linked to an increased risk for schizophrenia. The present study aimed to determine whether neonatal infection produced long-term disruptions in behaviour and pathology that might provide a parallel with that observed in schizophrenia. Rats were administered lipopolysaccharide (LPS; 500 microg/kg i.p.) on postnatal day 7 and 9. Locomotor activity and object recognition memory were tested at day 35 and day 70. LPS animals were observed to be less active at adulthood as measured by locomotor activity. With regards to object recognition memory, LPS administration produced no early impairment in task performance, however, at day 70 LPS animals spent significantly less time exploring the novel object than control animals. Analysis of brains showed a reduction in expression of parvalbumin immunoreactive neurons in the hippocampus of LPS animals with significant reductions selectively localised to the CA1-CA3 region, and not the dentate gyrus. No changes were observed in prefrontal cortex. These results show that neonatal LPS results in pathophysiological brain changes in hippocampal CA1-CA3 subregions.
    Behavioural brain research 08/2009; 205(2):355-9. DOI:10.1016/j.bbr.2009.07.014 · 3.39 Impact Factor
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