Viral infection, inflammation and schizophrenia
Identifieur interne : 000995 ( Main/Exploration ); précédent : 000994; suivant : 000996Viral infection, inflammation and schizophrenia
Auteurs : Rachel E. Kneeland [États-Unis] ; S. Hossein Fatemi [États-Unis]Source :
- Progress in neuro-psychopharmacology & biological psychiatry [ 0278-5846 ] ; 2012.
Abstract
Schizophrenia is a severe neurodevelopmental disorder with genetic and environmental etiologies. Prenatal viral/bacterial infections and inflammation play major roles in the genesis of schizophrenia. In this review, we describe a viral model of schizophrenia tested in mice whereby the offspring of mice prenatally infected with influenza at E7, E9, E16, and E18 show significant gene, protein, and brain structural abnormalities postnatally. Similarly, we describe data on rodents exposed to bacterial infection or injected with a synthetic viral mimic (PolyI:C) also demonstrating brain structural and behavioral abnormalities. Moreover, human serologic data has been indispensible in supporting the viral theory of schizophrenia. Individuals born seropositive for bacterial and viral agents are at a significantly elevated risk of developing schizophrenia. While the specific mechanisms of prenatal viral/bacterial infections and brain disorder are unclear, recent findings suggest that the maternal inflammatory response may be associated with fetal brain injury. Preventive and therapeutic treatment options are also proposed. This review presents data related to epidemiology, human serology, and experimental animal models which support the viral model of schizophrenia.
Url:
DOI: 10.1016/j.pnpbp.2012.02.001
PubMed: 22349576
PubMed Central: 3408569
Affiliations:
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Kneeland</name><affiliation wicri:level="2"><nlm:aff id="A1">Department of Psychiatry, Division of Neuroscience Research, University of Minnesota Medical School, 420 Delaware St. SE, MMC 392, Minneapolis, MN 55455, United States</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Psychiatry, Division of Neuroscience Research, University of Minnesota Medical School, 420 Delaware St. SE, MMC 392, Minneapolis, MN 55455</wicri:regionArea><placeName><region type="state">Minnesota</region></placeName></affiliation></author><author><name sortKey="Fatemi, S Hossein" sort="Fatemi, S Hossein" uniqKey="Fatemi S" first="S. Hossein" last="Fatemi">S. Hossein Fatemi</name><affiliation wicri:level="2"><nlm:aff id="A1">Department of Psychiatry, Division of Neuroscience Research, University of Minnesota Medical School, 420 Delaware St. SE, MMC 392, Minneapolis, MN 55455, United States</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Psychiatry, Division of Neuroscience Research, University of Minnesota Medical School, 420 Delaware St. SE, MMC 392, Minneapolis, MN 55455</wicri:regionArea><placeName><region type="state">Minnesota</region></placeName></affiliation><affiliation wicri:level="2"><nlm:aff id="A2">Department of Pharmacology, University of Minnesota Medical School, 310 Church St. SE, Minneapolis, MN 55455, United States and Department of Neuroscience, University of Minnesota Medical School, 310 Church St. SE, Minneapolis, MN 55455, United States</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pharmacology, University of Minnesota Medical School, 310 Church St. SE, Minneapolis, MN 55455, United States and Department of Neuroscience, University of Minnesota Medical School, 310 Church St. SE, Minneapolis, MN 55455</wicri:regionArea><placeName><region type="state">Minnesota</region></placeName></affiliation></author></analytic><series><title level="j">Progress in neuro-psychopharmacology & biological psychiatry</title><idno type="ISSN">0278-5846</idno><idno type="eISSN">1878-4216</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Schizophrenia is a severe neurodevelopmental disorder with genetic and environmental etiologies. Prenatal viral/bacterial infections and inflammation play major roles in the genesis of schizophrenia. In this review, we describe a viral model of schizophrenia tested in mice whereby the offspring of mice prenatally infected with influenza at E7, E9, E16, and E18 show significant gene, protein, and brain structural abnormalities postnatally. Similarly, we describe data on rodents exposed to bacterial infection or injected with a synthetic viral mimic (PolyI:C) also demonstrating brain structural and behavioral abnormalities. Moreover, human serologic data has been indispensible in supporting the viral theory of schizophrenia. Individuals born seropositive for bacterial and viral agents are at a significantly elevated risk of developing schizophrenia. While the specific mechanisms of prenatal viral/bacterial infections and brain disorder are unclear, recent findings suggest that the maternal inflammatory response may be associated with fetal brain injury. Preventive and therapeutic treatment options are also proposed. This review presents data related to epidemiology, human serology, and experimental animal models which support the viral model of schizophrenia.</p></div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Minnesota</li></region></list><tree><country name="États-Unis"><region name="Minnesota"><name sortKey="Kneeland, Rachel E" sort="Kneeland, Rachel E" uniqKey="Kneeland R" first="Rachel E." last="Kneeland">Rachel E. Kneeland</name></region><name sortKey="Fatemi, S Hossein" sort="Fatemi, S Hossein" uniqKey="Fatemi S" first="S. Hossein" last="Fatemi">S. Hossein Fatemi</name><name sortKey="Fatemi, S Hossein" sort="Fatemi, S Hossein" uniqKey="Fatemi S" first="S. Hossein" last="Fatemi">S. Hossein Fatemi</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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