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Epidemiology-driven neurodevelopmental animal models of schizophrenia.
Prog Neurobiol 2010; 90(3):285-326PN

Abstract

Human epidemiological studies have provided compelling evidence that the risk of developing schizophrenia is significantly enhanced following prenatal and/or perinatal exposure to various environmental insults, including maternal exposure to stress, infection and/or immune activation, nutritional deficiencies and obstetric complications. Based on these associations, a great deal of interest has been centered upon the establishment of neurodevelopmental animal models which are based on prenatal and/or perinatal exposure to such environmental stimuli. In the present review, we describe this relatively novel class of epidemiology-based animal models in relation to the etiology, neurobiology and psychopharmacology of schizophrenia. Thereby, we discuss the general design and practical implementation of these models, and we provide an integrative summary of experimental findings derived from diverse epidemiology-based models, including models of maternal exposure to psychological stress, glucocorticoid treatment, viral infection, immune activating agents, protein deprivation, vitamin D deficiency, as well as models of obstetric complications in the form of birth by Caesarian section and perinatal/postnatal hypoxia. We highlight that the long-term consequences of prenatal exposure to these environmental challenges in animals successfully capture a broad spectrum of structural and functional brain abnormalities implicated in schizophrenia, some of which can be normalized by acute and/or chronic antipsychotic drug treatment. We thus conclude that epidemiology-driven neurodevelopmental models of schizophrenia are characterized by a high level of face, construct and predictive validity, including intrinsic etiological significance to the disorder. They also fulfill the expectation of the neurodevelopmental theory, such that the effects of prenatal environmental insults often only emerge after puberty. Epidemiologically based animal models not only provide indispensable experimental tools to test the hypothesis of causality in human epidemiological associations, but they also offer important new avenues for the elucidation of neurobiological, neuroendocrine and neuroimmunological mechanisms involved in the etiopathogenesis of schizophrenia and related disorders.

Authors+Show Affiliations

Laboratory of Behavioural Neurobiology, Swiss Federal Institute of Technology (ETH) Zurich, Schorenstrasse 16, CH-8603 Schwerzenbach, Switzerland. urmeyer@ethz.chNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

19857543

Citation

Meyer, Urs, and Joram Feldon. "Epidemiology-driven Neurodevelopmental Animal Models of Schizophrenia." Progress in Neurobiology, vol. 90, no. 3, 2010, pp. 285-326.
Meyer U, Feldon J. Epidemiology-driven neurodevelopmental animal models of schizophrenia. Prog Neurobiol. 2010;90(3):285-326.
Meyer, U., & Feldon, J. (2010). Epidemiology-driven neurodevelopmental animal models of schizophrenia. Progress in Neurobiology, 90(3), pp. 285-326. doi:10.1016/j.pneurobio.2009.10.018.
Meyer U, Feldon J. Epidemiology-driven Neurodevelopmental Animal Models of Schizophrenia. Prog Neurobiol. 2010;90(3):285-326. PubMed PMID: 19857543.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Epidemiology-driven neurodevelopmental animal models of schizophrenia. AU - Meyer,Urs, AU - Feldon,Joram, Y1 - 2009/10/24/ PY - 2009/07/28/received PY - 2009/09/30/revised PY - 2009/10/14/accepted PY - 2009/10/28/entrez PY - 2009/10/28/pubmed PY - 2010/6/16/medline SP - 285 EP - 326 JF - Progress in neurobiology JO - Prog. Neurobiol. VL - 90 IS - 3 N2 - Human epidemiological studies have provided compelling evidence that the risk of developing schizophrenia is significantly enhanced following prenatal and/or perinatal exposure to various environmental insults, including maternal exposure to stress, infection and/or immune activation, nutritional deficiencies and obstetric complications. Based on these associations, a great deal of interest has been centered upon the establishment of neurodevelopmental animal models which are based on prenatal and/or perinatal exposure to such environmental stimuli. In the present review, we describe this relatively novel class of epidemiology-based animal models in relation to the etiology, neurobiology and psychopharmacology of schizophrenia. Thereby, we discuss the general design and practical implementation of these models, and we provide an integrative summary of experimental findings derived from diverse epidemiology-based models, including models of maternal exposure to psychological stress, glucocorticoid treatment, viral infection, immune activating agents, protein deprivation, vitamin D deficiency, as well as models of obstetric complications in the form of birth by Caesarian section and perinatal/postnatal hypoxia. We highlight that the long-term consequences of prenatal exposure to these environmental challenges in animals successfully capture a broad spectrum of structural and functional brain abnormalities implicated in schizophrenia, some of which can be normalized by acute and/or chronic antipsychotic drug treatment. We thus conclude that epidemiology-driven neurodevelopmental models of schizophrenia are characterized by a high level of face, construct and predictive validity, including intrinsic etiological significance to the disorder. They also fulfill the expectation of the neurodevelopmental theory, such that the effects of prenatal environmental insults often only emerge after puberty. Epidemiologically based animal models not only provide indispensable experimental tools to test the hypothesis of causality in human epidemiological associations, but they also offer important new avenues for the elucidation of neurobiological, neuroendocrine and neuroimmunological mechanisms involved in the etiopathogenesis of schizophrenia and related disorders. SN - 1873-5118 UR - https://www.unboundmedicine.com/medline/citation/19857543/Epidemiology_driven_neurodevelopmental_animal_models_of_schizophrenia_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0301-0082(09)00169-5 DB - PRIME DP - Unbound Medicine ER -