PoplarV1, Main, Exploration, bibRecord, 001A24

A review of vulnerability and risks for schizophrenia: Beyond the two hit hypothesis.

Identifieur interne : 001A24 ( Main/Exploration ); précédent : 001A23; suivant : 001A25

A review of vulnerability and risks for schizophrenia: Beyond the two hit hypothesis.

Auteurs : Justin Davis [Australie] ; Harris Eyre [Australie] ; Felice N. Jacka [Australie] ; Seetal Dodd [Australie] ; Olivia Dean [Australie] ; Sarah Mcewen [États-Unis] ; Monojit Debnath [Inde] ; John Mcgrath [Australie] ; Michael Maes [Australie] ; Paul Amminger [Australie] ; Patrick D. Mcgorry [Australie] ; Christos Pantelis [Australie] ; Michael Berk [Australie]

Source :

Neuroscience and biobehavioral reviews [ 1873-7528 ] ; 2016.

RBID : pubmed:27073049

Descripteurs français

KwdFr :
- Environnement (MeSH), Facteurs de risque (MeSH), Humains (MeSH), Phénotype (MeSH), Prédisposition génétique à une maladie (MeSH), Schizophrénie (MeSH).
MESH :
- Environnement, Facteurs de risque, Humains, Phénotype, Prédisposition génétique à une maladie, Schizophrénie.

English descriptors

KwdEn :
- Environment (MeSH), Genetic Predisposition to Disease (MeSH), Humans (MeSH), Phenotype (MeSH), Risk Factors (MeSH), Schizophrenia (MeSH).
MESH :
- Environment, Genetic Predisposition to Disease, Humans, Phenotype, Risk Factors, Schizophrenia.

Abstract

Schizophrenia risk has often been conceptualized using a model which requires two hits in order to generate the clinical phenotype-the first as an early priming in a genetically predisposed individual and the second a likely environmental insult. The aim of this paper was to review the literature and reformulate this binary risk-vulnerability model. We sourced the data for this narrative review from the electronic database PUBMED. Our search terms were not limited by language or date of publication. The development of schizophrenia may be driven by genetic vulnerability interacting with multiple vulnerability factors including lowered prenatal vitamin D exposure, viral infections, smoking intelligence quotient, social cognition cannabis use, social defeat, nutrition and childhood trauma. It is likely that these genetic risks, environmental risks and vulnerability factors are cumulative and interactive with each other and with critical periods of neurodevelopmental vulnerability. The development of schizophrenia is likely to be more complex and nuanced than the binary two hit model originally proposed nearly thirty years ago. Risk appears influenced by a more complex process involving genetic risk interfacing with multiple potentially interacting hits and vulnerability factors occurring at key periods of neurodevelopmental activity, which culminate in the expression of disease state. These risks are common across a number of neuropsychiatric and medical disorders, which might inform common preventive and intervention strategies across non-communicable disorders.

DOI: 10.1016/j.neubiorev.2016.03.017
PubMed: 27073049
PubMed Central: PMC4876729

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Environment (MeSH)</term>
<term>Genetic Predisposition to Disease (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Phenotype (MeSH)</term>
<term>Risk Factors (MeSH)</term>
<term>Schizophrenia (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Environnement (MeSH)</term>
<term>Facteurs de risque (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Phénotype (MeSH)</term>
<term>Prédisposition génétique à une maladie (MeSH)</term>
<term>Schizophrénie (MeSH)</term>
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<keywords scheme="MESH" xml:lang="en"><term>Environment</term>
<term>Genetic Predisposition to Disease</term>
<term>Humans</term>
<term>Phenotype</term>
<term>Risk Factors</term>
<term>Schizophrenia</term>
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<term>Facteurs de risque</term>
<term>Humains</term>
<term>Phénotype</term>
<term>Prédisposition génétique à une maladie</term>
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<front><div type="abstract" xml:lang="en">Schizophrenia risk has often been conceptualized using a model which requires two hits in order to generate the clinical phenotype-the first as an early priming in a genetically predisposed individual and the second a likely environmental insult. The aim of this paper was to review the literature and reformulate this binary risk-vulnerability model. We sourced the data for this narrative review from the electronic database PUBMED. Our search terms were not limited by language or date of publication. The development of schizophrenia may be driven by genetic vulnerability interacting with multiple vulnerability factors including lowered prenatal vitamin D exposure, viral infections, smoking intelligence quotient, social cognition cannabis use, social defeat, nutrition and childhood trauma. It is likely that these genetic risks, environmental risks and vulnerability factors are cumulative and interactive with each other and with critical periods of neurodevelopmental vulnerability. The development of schizophrenia is likely to be more complex and nuanced than the binary two hit model originally proposed nearly thirty years ago. Risk appears influenced by a more complex process involving genetic risk interfacing with multiple potentially interacting hits and vulnerability factors occurring at key periods of neurodevelopmental activity, which culminate in the expression of disease state. These risks are common across a number of neuropsychiatric and medical disorders, which might inform common preventive and intervention strategies across non-communicable disorders.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" IndexingMethod="Curated" Owner="NLM"><PMID Version="1">27073049</PMID>
<DateCompleted><Year>2017</Year>
<Month>10</Month>
<Day>19</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>03</Month>
<Day>06</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-7528</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>65</Volume>
<PubDate><Year>2016</Year>
<Month>Jun</Month>
</PubDate>
</JournalIssue>
<Title>Neuroscience and biobehavioral reviews</Title>
<ISOAbbreviation>Neurosci Biobehav Rev</ISOAbbreviation>
</Journal>
<ArticleTitle>A review of vulnerability and risks for schizophrenia: Beyond the two hit hypothesis.</ArticleTitle>
<Pagination><MedlinePgn>185-94</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.neubiorev.2016.03.017</ELocationID>
<ELocationID EIdType="pii" ValidYN="Y">S0149-7634(15)30294-3</ELocationID>
<Abstract><AbstractText>Schizophrenia risk has often been conceptualized using a model which requires two hits in order to generate the clinical phenotype-the first as an early priming in a genetically predisposed individual and the second a likely environmental insult. The aim of this paper was to review the literature and reformulate this binary risk-vulnerability model. We sourced the data for this narrative review from the electronic database PUBMED. Our search terms were not limited by language or date of publication. The development of schizophrenia may be driven by genetic vulnerability interacting with multiple vulnerability factors including lowered prenatal vitamin D exposure, viral infections, smoking intelligence quotient, social cognition cannabis use, social defeat, nutrition and childhood trauma. It is likely that these genetic risks, environmental risks and vulnerability factors are cumulative and interactive with each other and with critical periods of neurodevelopmental vulnerability. The development of schizophrenia is likely to be more complex and nuanced than the binary two hit model originally proposed nearly thirty years ago. Risk appears influenced by a more complex process involving genetic risk interfacing with multiple potentially interacting hits and vulnerability factors occurring at key periods of neurodevelopmental activity, which culminate in the expression of disease state. These risks are common across a number of neuropsychiatric and medical disorders, which might inform common preventive and intervention strategies across non-communicable disorders.</AbstractText>
<CopyrightInformation>Copyright © 2016 Elsevier Ltd. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Davis</LastName>
<ForeName>Justin</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Deakin University, IMPACT Strategic Research Centre, School of Medicine, Barwon Health, P.O. Box 291, Geelong, 3220, Australia. Electronic address: justinbdavis19@gmail.com.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Eyre</LastName>
<ForeName>Harris</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Deakin University, IMPACT Strategic Research Centre, School of Medicine, Barwon Health, P.O. Box 291, Geelong, 3220, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Jacka</LastName>
<ForeName>Felice N</ForeName>
<Initials>FN</Initials>
<AffiliationInfo><Affiliation>Deakin University, IMPACT Strategic Research Centre, School of Medicine, Barwon Health, P.O. Box 291, Geelong, 3220, Australia; University of Melbourne, Department of Psychiatry, Level 1 North, Main Block, Royal Melbourne Hospital, Parkville, 3052, Australia; Centre for Adolescent Health, Murdoch Children's Research Institute, Melbourne, Australia; Black Dog Institute, Sydney, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Dodd</LastName>
<ForeName>Seetal</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Deakin University, IMPACT Strategic Research Centre, School of Medicine, Barwon Health, P.O. Box 291, Geelong, 3220, Australia; University of Melbourne, Department of Psychiatry, Level 1 North, Main Block, Royal Melbourne Hospital, Parkville, 3052, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Dean</LastName>
<ForeName>Olivia</ForeName>
<Initials>O</Initials>
<AffiliationInfo><Affiliation>Deakin University, IMPACT Strategic Research Centre, School of Medicine, Barwon Health, P.O. Box 291, Geelong, 3220, Australia; University of Melbourne, Department of Psychiatry, Level 1 North, Main Block, Royal Melbourne Hospital, Parkville, 3052, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>McEwen</LastName>
<ForeName>Sarah</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Semel Institute for Neuroscience and Human Behavior, UCLA, United States.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Debnath</LastName>
<ForeName>Monojit</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Human Genetics, National Institute of Mental Health and Neurosciences, Bangalore, India.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>McGrath</LastName>
<ForeName>John</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Queensland Brain Institute, The University of Queensland, Brisbane, 4072, Queensland, Australia; Queensland Centre for Mental Health Research, The Park Centre for Mental Health, Wacol, Queensland 4076, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Maes</LastName>
<ForeName>Michael</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Deakin University, IMPACT Strategic Research Centre, School of Medicine, Barwon Health, P.O. Box 291, Geelong, 3220, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Amminger</LastName>
<ForeName>Paul</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Queensland Brain Institute, The University of Queensland, Brisbane, 4072, Queensland, Australia; Orygen, The National Centre of Excellence in Youth Mental Health and Orygen Youth Health Research Centre, 35 Poplar Rd., Parkville, 3052, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>McGorry</LastName>
<ForeName>Patrick D</ForeName>
<Initials>PD</Initials>
<AffiliationInfo><Affiliation>Orygen, The National Centre of Excellence in Youth Mental Health and Orygen Youth Health Research Centre, 35 Poplar Rd., Parkville, 3052, Australia; Centre of Youth Mental Health, University of Melbourne, 35 Poplar Rd., Parkville, 3052, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Pantelis</LastName>
<ForeName>Christos</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>University of Melbourne, Department of Psychiatry, Level 1 North, Main Block, Royal Melbourne Hospital, Parkville, 3052, Australia; Department of Human Genetics, National Institute of Mental Health and Neurosciences, Bangalore, India; Melbourne Neuropsychiatry Centre, The University of Melbourne & Melbourne Health, Parkville, 3052, Australia; Florey Institute for Neuroscience and Mental Health, University of Melbourne, Kenneth Myer Building, 30 Royal Parade, 3052, Parkville, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Berk</LastName>
<ForeName>Michael</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Deakin University, IMPACT Strategic Research Centre, School of Medicine, Barwon Health, P.O. Box 291, Geelong, 3220, Australia; University of Melbourne, Department of Psychiatry, Level 1 North, Main Block, Royal Melbourne Hospital, Parkville, 3052, Australia; Queensland Centre for Mental Health Research, The Park Centre for Mental Health, Wacol, Queensland 4076, Australia; Orygen, The National Centre of Excellence in Youth Mental Health and Orygen Youth Health Research Centre, 35 Poplar Rd., Parkville, 3052, Australia; Centre of Youth Mental Health, University of Melbourne, 35 Poplar Rd., Parkville, 3052, Australia; Florey Institute for Neuroscience and Mental Health, University of Melbourne, Kenneth Myer Building, 30 Royal Parade, 3052, Parkville, Australia.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>K01 MH099431</GrantID>
<Acronym>MH</Acronym>
<Agency>NIMH NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D016454">Review</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2016</Year>
<Month>04</Month>
<Day>09</Day>
</ArticleDate>
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<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Neurosci Biobehav Rev</MedlineTA>
<NlmUniqueID>7806090</NlmUniqueID>
<ISSNLinking>0149-7634</ISSNLinking>
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<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D004777" MajorTopicYN="N">Environment</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020022" MajorTopicYN="N">Genetic Predisposition to Disease</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010641" MajorTopicYN="N">Phenotype</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012559" MajorTopicYN="Y">Schizophrenia</DescriptorName>
</MeshHeading>
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<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year>
<Month>11</Month>
<Day>18</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2016</Year>
<Month>03</Month>
<Day>25</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2016</Year>
<Month>03</Month>
<Day>25</Day>
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<Month>4</Month>
<Day>14</Day>
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A review of vulnerability and risks for schizophrenia: Beyond the two hit hypothesis.

A review of vulnerability and risks for schizophrenia: Beyond the two hit hypothesis.

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