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Article: The timing and specificity of prenatal immune risk factors for autism modeled in the mouse and relevance to schizophrenia

TitleThe timing and specificity of prenatal immune risk factors for autism modeled in the mouse and relevance to schizophrenia
Authors
KeywordsAutism
Infection
Inflammation
Mouse model
Pregnancy
Prenatal infection
Schizophrenia
Issue Date2011
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSG
Citation
Neurosignals, 2011, v. 18 n. 2, p. 129-139 How to Cite?
AbstractAutism is a highly heritable condition, but there is strong epidemiological evidence that environmental factors, especially prenatal exposure to immune challenge, contribute to it. This evidence is largely indirect, and experimental testing is necessary to directly examine causal mechanisms. Mouse models reveal that prenatal immune perturbation disrupts postnatal brain maturation with alterations in gene and protein expression, neurotransmitter function, brain structure and behavioral indices reminiscent of, but not specific to, autism. This likely reflects a neurodevelopmental spectrum in which autism and schizophrenia share numerous genetic and environmental risk factors for difficulties in social interaction, communication, emotion processing and executive function. Recent epidemiological studies find that early rather than late pregnancy infection confers the greater risk of schizophrenia. The autism literature is more limited, but exposures in the 2nd half of pregnancy may be important. Mouse models of prenatal immune challenge help dissect these observations and show some common consequences of early and late gestational exposures, as well as distinct ramifications potentially relevant to schizophrenia and autism. Although nonspecificity of immune-stimulated mouse models could be considered a disadvantage, we propose a broadened perspective, exploiting the possibility that advances made investigating a target condition can contribute towards the understanding of related conditions. Copyright © 2010 S. Karger AG.
Persistent Identifierhttp://hdl.handle.net/10722/135409
ISSN
2015 Impact Factor: 1.593
2015 SCImago Journal Rankings: 0.763
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMcAlonan, GMen_HK
dc.contributor.authorLi, Qen_HK
dc.contributor.authorCheung, Cen_HK
dc.date.accessioned2011-07-27T01:34:49Z-
dc.date.available2011-07-27T01:34:49Z-
dc.date.issued2011en_HK
dc.identifier.citationNeurosignals, 2011, v. 18 n. 2, p. 129-139en_HK
dc.identifier.issn1424-862Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/135409-
dc.description.abstractAutism is a highly heritable condition, but there is strong epidemiological evidence that environmental factors, especially prenatal exposure to immune challenge, contribute to it. This evidence is largely indirect, and experimental testing is necessary to directly examine causal mechanisms. Mouse models reveal that prenatal immune perturbation disrupts postnatal brain maturation with alterations in gene and protein expression, neurotransmitter function, brain structure and behavioral indices reminiscent of, but not specific to, autism. This likely reflects a neurodevelopmental spectrum in which autism and schizophrenia share numerous genetic and environmental risk factors for difficulties in social interaction, communication, emotion processing and executive function. Recent epidemiological studies find that early rather than late pregnancy infection confers the greater risk of schizophrenia. The autism literature is more limited, but exposures in the 2nd half of pregnancy may be important. Mouse models of prenatal immune challenge help dissect these observations and show some common consequences of early and late gestational exposures, as well as distinct ramifications potentially relevant to schizophrenia and autism. Although nonspecificity of immune-stimulated mouse models could be considered a disadvantage, we propose a broadened perspective, exploiting the possibility that advances made investigating a target condition can contribute towards the understanding of related conditions. Copyright © 2010 S. Karger AG.en_HK
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSGen_HK
dc.relation.ispartofNeuroSignalsen_HK
dc.rightsNeurosignals. Copyright © S Karger AG.-
dc.subjectAutismen_HK
dc.subjectInfectionen_HK
dc.subjectInflammationen_HK
dc.subjectMouse modelen_HK
dc.subjectPregnancyen_HK
dc.subjectPrenatal infectionen_HK
dc.subjectSchizophreniaen_HK
dc.subject.meshAutistic Disorder - etiology-
dc.subject.meshImmunologic Factors - adverse effects-
dc.subject.meshPregnancy-
dc.subject.meshPrenatal Exposure Delayed Effects-
dc.subject.meshSchizophrenia - etiology-
dc.titleThe timing and specificity of prenatal immune risk factors for autism modeled in the mouse and relevance to schizophreniaen_HK
dc.typeArticleen_HK
dc.identifier.emailMcAlonan, GM: mcalonan@hkucc.hku.hken_HK
dc.identifier.emailCheung, C: charlton@hkucc.hku.hken_HK
dc.identifier.authorityMcAlonan, GM=rp00475en_HK
dc.identifier.authorityCheung, C=rp01574en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1159/000321080en_HK
dc.identifier.pmid21042002-
dc.identifier.scopuseid_2-s2.0-79952444133en_HK
dc.identifier.hkuros187264en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79952444133&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume18en_HK
dc.identifier.issue2en_HK
dc.identifier.spage129en_HK
dc.identifier.epage139en_HK
dc.identifier.isiWOS:000287794500007-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridMcAlonan, GM=6603123011en_HK
dc.identifier.scopusauthoridLi, Q=36065644400en_HK
dc.identifier.scopusauthoridCheung, C=7202061845en_HK
dc.identifier.citeulike9645022-

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