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Auteur D. M. ALLSWEDE |
Documents disponibles écrits par cet auteur (1)
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Prenatal inflammation and risk for schizophrenia: A role for immune proteins in neurodevelopment / D. M. ALLSWEDE in Development and Psychopathology, 30-3 (August 2018)
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Titre : Prenatal inflammation and risk for schizophrenia: A role for immune proteins in neurodevelopment Type de document : Texte imprimé et/ou numérique Auteurs : D. M. ALLSWEDE, Auteur ; Tyrone D. CANNON, Auteur Article en page(s) : p.1157-1178 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Prenatal inflammation is an established risk factor for schizophrenia. However, the specific inflammatory pathways that mediate this association remain unclear. Potential candidate systems include inflammatory markers produced by microglia, such as cytokines and complement. Accumulating evidence suggests that these markers play a role in typical neurodevelopmental processes, such as synapse formation and interneuron migration. Rodent models demonstrate that altered marker levels during the prenatal period can cause lasting deficits in these systems, leading to cognitive deficits that resemble schizophrenia. This review assesses the potential role of prenatal cytokine and complement elevations on the etiology of schizophrenia. The current neurobiological understanding of the development of schizophrenia is reviewed to identify candidate cellular mechanisms that may be influenced by prenatal inflammation. We discuss the functions that cytokines and complement may play in prenatal neurodevelopment, review evidence that links exposure to these factors with risk for schizophrenia, and consider how these markers may interact with genetic vulnerabilities to influence the neurodevelopment of schizophrenia. We consider how prenatal inflammatory exposure may influence childhood and adolescent developmental risk trajectories for schizophrenia. Finally, we identify areas of further research needed to support the development of anti-inflammatory treatments to prevent the development of schizophrenia in at-risk neonates. En ligne : http://dx.doi.org/10.1017/s0954579418000317 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367
in Development and Psychopathology > 30-3 (August 2018) . - p.1157-1178[article] Prenatal inflammation and risk for schizophrenia: A role for immune proteins in neurodevelopment [Texte imprimé et/ou numérique] / D. M. ALLSWEDE, Auteur ; Tyrone D. CANNON, Auteur . - p.1157-1178.
Langues : Anglais (eng)
in Development and Psychopathology > 30-3 (August 2018) . - p.1157-1178
Index. décimale : PER Périodiques Résumé : Prenatal inflammation is an established risk factor for schizophrenia. However, the specific inflammatory pathways that mediate this association remain unclear. Potential candidate systems include inflammatory markers produced by microglia, such as cytokines and complement. Accumulating evidence suggests that these markers play a role in typical neurodevelopmental processes, such as synapse formation and interneuron migration. Rodent models demonstrate that altered marker levels during the prenatal period can cause lasting deficits in these systems, leading to cognitive deficits that resemble schizophrenia. This review assesses the potential role of prenatal cytokine and complement elevations on the etiology of schizophrenia. The current neurobiological understanding of the development of schizophrenia is reviewed to identify candidate cellular mechanisms that may be influenced by prenatal inflammation. We discuss the functions that cytokines and complement may play in prenatal neurodevelopment, review evidence that links exposure to these factors with risk for schizophrenia, and consider how these markers may interact with genetic vulnerabilities to influence the neurodevelopment of schizophrenia. We consider how prenatal inflammatory exposure may influence childhood and adolescent developmental risk trajectories for schizophrenia. Finally, we identify areas of further research needed to support the development of anti-inflammatory treatments to prevent the development of schizophrenia in at-risk neonates. En ligne : http://dx.doi.org/10.1017/s0954579418000317 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367