[Biological hypotheses of schizophrenia: possible influences of immunology and endocrinology].
Identifieur interne : 000864 ( PubMed/Corpus ); précédent : 000863; suivant : 000865[Biological hypotheses of schizophrenia: possible influences of immunology and endocrinology].
Auteurs : B. Sperner-UnterwegerSource :
- Fortschritte der Neurologie-Psychiatrie [ 0720-4299 ] ; 2005.
English descriptors
- KwdEn :
- MESH :
- etiology : Schizophrenia.
- immunology : Schizophrenia.
- physiopathology : Endocrine Glands, Schizophrenia.
- Humans.
Abstract
A great number of studies show biological alterations in patients with schizophrenia, but many of these data are conflicting. Schizophrenia is a vastly heterogeneous disorder, most likely not caused by one etiological factor, but rather due to a complex network of different, interacting pathogenic influences. Variable clinical pictures may reflect different etiological factors. In a comprehensive theory of the origin of schizophrenic disorders, genetic and environmental influences cause changes in neuronal development which result in functional alterations of different neurotransmitter systems. Immunological research in schizophrenia was initially based on the "infection hypothesis" which was triggered by observing schizophrenia-like psychoses after influenza pandemic. Numerous immunological studies focusing on antibodies against specific viruses, unspecific antibodies and different other immune-phenomena were carried out in schizophrenia patients. Although the variability of the results from these studies is strikingly high, subgroups of patients with schizophrenia show an activated inflammatory response system with increased levels of proinflammatory cytokines and acute phase proteins. Furthermore, some investigations find changing activities in the T-cell system with a shift of TH-1 to an increased TH-2 activity. Endocrinological factors which may play a relevant role in the etiopathogenesis of schizophrenia include sex hormones and all changes caused by stress or other influences which are directly related to the HPA-axis. Alterations of the immune and the endocrinological systems might be caused by environmental factors like infections or exogenous stress. Due to the intensive interaction between the central nervous system, the immune system and different hormones the "development of a pathology" like schizophrenia can be seen in an integrative but multifactorial fashion. The clinical manifestation, the severity and the course of the disease might then be modulated by genetic vulnerability, the time of the "primary insult" -- which could be an infection, or psychological stress -- and its neuronal localisation and intensity. Different compensatory and decompensatory mechanisms in later life very likely play a crucial role for the further course of the disorder.
DOI: 10.1055/s-2005-915544
PubMed: 16270243
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Sperner-Unterweger</name><affiliation><nlm:affiliation>Abteilung für Biologische Psychiatrie, Univ.-Klinik für Psychiatrie Innsbruck/Osterreich. barbara.sperner-unterweger@uibk.ac.at</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="RBID">pubmed:16270243</idno><idno type="pmid">16270243</idno><idno type="doi">10.1055/s-2005-915544</idno><idno type="wicri:Area/PubMed/Corpus">000864</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000864</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">[Biological hypotheses of schizophrenia: possible influences of immunology and endocrinology].</title><author><name sortKey="Sperner Unterweger, B" sort="Sperner Unterweger, B" uniqKey="Sperner Unterweger B" first="B" last="Sperner-Unterweger">B. Sperner-Unterweger</name><affiliation><nlm:affiliation>Abteilung für Biologische Psychiatrie, Univ.-Klinik für Psychiatrie Innsbruck/Osterreich. barbara.sperner-unterweger@uibk.ac.at</nlm:affiliation></affiliation></author></analytic><series><title level="j">Fortschritte der Neurologie-Psychiatrie</title><idno type="ISSN">0720-4299</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Endocrine Glands (physiopathology)</term><term>Humans</term><term>Schizophrenia (etiology)</term><term>Schizophrenia (immunology)</term><term>Schizophrenia (physiopathology)</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Schizophrenia</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Schizophrenia</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Endocrine Glands</term><term>Schizophrenia</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A great number of studies show biological alterations in patients with schizophrenia, but many of these data are conflicting. Schizophrenia is a vastly heterogeneous disorder, most likely not caused by one etiological factor, but rather due to a complex network of different, interacting pathogenic influences. Variable clinical pictures may reflect different etiological factors. In a comprehensive theory of the origin of schizophrenic disorders, genetic and environmental influences cause changes in neuronal development which result in functional alterations of different neurotransmitter systems. Immunological research in schizophrenia was initially based on the "infection hypothesis" which was triggered by observing schizophrenia-like psychoses after influenza pandemic. Numerous immunological studies focusing on antibodies against specific viruses, unspecific antibodies and different other immune-phenomena were carried out in schizophrenia patients. Although the variability of the results from these studies is strikingly high, subgroups of patients with schizophrenia show an activated inflammatory response system with increased levels of proinflammatory cytokines and acute phase proteins. Furthermore, some investigations find changing activities in the T-cell system with a shift of TH-1 to an increased TH-2 activity. Endocrinological factors which may play a relevant role in the etiopathogenesis of schizophrenia include sex hormones and all changes caused by stress or other influences which are directly related to the HPA-axis. Alterations of the immune and the endocrinological systems might be caused by environmental factors like infections or exogenous stress. Due to the intensive interaction between the central nervous system, the immune system and different hormones the "development of a pathology" like schizophrenia can be seen in an integrative but multifactorial fashion. The clinical manifestation, the severity and the course of the disease might then be modulated by genetic vulnerability, the time of the "primary insult" -- which could be an infection, or psychological stress -- and its neuronal localisation and intensity. Different compensatory and decompensatory mechanisms in later life very likely play a crucial role for the further course of the disorder.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16270243</PMID><DateCompleted><Year>2006</Year><Month>01</Month><Day>05</Day></DateCompleted><DateRevised><Year>2006</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0720-4299</ISSN><JournalIssue CitedMedium="Print"><Volume>73 Suppl 1</Volume><PubDate><Year>2005</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Fortschritte der Neurologie-Psychiatrie</Title><ISOAbbreviation>Fortschr Neurol Psychiatr</ISOAbbreviation></Journal><ArticleTitle>[Biological hypotheses of schizophrenia: possible influences of immunology and endocrinology].</ArticleTitle><Pagination><MedlinePgn>S38-43</MedlinePgn></Pagination><Abstract><AbstractText>A great number of studies show biological alterations in patients with schizophrenia, but many of these data are conflicting. Schizophrenia is a vastly heterogeneous disorder, most likely not caused by one etiological factor, but rather due to a complex network of different, interacting pathogenic influences. Variable clinical pictures may reflect different etiological factors. In a comprehensive theory of the origin of schizophrenic disorders, genetic and environmental influences cause changes in neuronal development which result in functional alterations of different neurotransmitter systems. Immunological research in schizophrenia was initially based on the "infection hypothesis" which was triggered by observing schizophrenia-like psychoses after influenza pandemic. Numerous immunological studies focusing on antibodies against specific viruses, unspecific antibodies and different other immune-phenomena were carried out in schizophrenia patients. Although the variability of the results from these studies is strikingly high, subgroups of patients with schizophrenia show an activated inflammatory response system with increased levels of proinflammatory cytokines and acute phase proteins. Furthermore, some investigations find changing activities in the T-cell system with a shift of TH-1 to an increased TH-2 activity. Endocrinological factors which may play a relevant role in the etiopathogenesis of schizophrenia include sex hormones and all changes caused by stress or other influences which are directly related to the HPA-axis. Alterations of the immune and the endocrinological systems might be caused by environmental factors like infections or exogenous stress. Due to the intensive interaction between the central nervous system, the immune system and different hormones the "development of a pathology" like schizophrenia can be seen in an integrative but multifactorial fashion. The clinical manifestation, the severity and the course of the disease might then be modulated by genetic vulnerability, the time of the "primary insult" -- which could be an infection, or psychological stress -- and its neuronal localisation and intensity. Different compensatory and decompensatory mechanisms in later life very likely play a crucial role for the further course of the disorder.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sperner-Unterweger</LastName><ForeName>B</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Abteilung für Biologische Psychiatrie, Univ.-Klinik für Psychiatrie Innsbruck/Osterreich. barbara.sperner-unterweger@uibk.ac.at</Affiliation></AffiliationInfo></Author></AuthorList><Language>ger</Language><PublicationTypeList><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><VernacularTitle>Biologische Hypothesen zur Schizophrenie: Mögliche Einflüsse von Immunologie und Endokrinologie.</VernacularTitle></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Fortschr Neurol Psychiatr</MedlineTA><NlmUniqueID>8103137</NlmUniqueID><ISSNLinking>0720-4299</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D004702" MajorTopicYN="N">Endocrine Glands</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012559" MajorTopicYN="N">Schizophrenia</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>52</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>11</Month><Day>5</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>1</Month><Day>6</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2005</Year><Month>11</Month><Day>5</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16270243</ArticleId><ArticleId IdType="doi">10.1055/s-2005-915544</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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