The BDNF Val66Met polymorphism moderates the relationship between cognitive reserve and executive function.
Identifieur interne : 002C40 ( PubMed/Corpus ); précédent : 002C39; suivant : 002C41The BDNF Val66Met polymorphism moderates the relationship between cognitive reserve and executive function.
Auteurs : D D Ward ; M J Summers ; N L Saunders ; K. Ritchie ; J J Summers ; J C VickersSource :
- Translational psychiatry [ 2158-3188 ] ; 2015.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Apolipoproteins E, Brain-Derived Neurotrophic Factor.
- Aged, Cognition, Cognitive Reserve, Executive Function, Female, Humans, Male, Middle Aged, Polymorphism, Genetic.
Abstract
The concept of cognitive reserve (CR) has been proposed to account for observed discrepancies between pathology and its clinical manifestation due to underlying differences in brain structure and function. In 433 healthy older adults participating in the Tasmanian Healthy Brain Project, we investigated whether common polymorphic variations in apolipoprotein E (APOE) or brain-derived neurotrophic factor (BDNF) influenced the association between CR contributors and cognitive function in older adults. We show that BDNF Val66Met moderates the association between CR and executive function. CR accounted for 8.5% of the variance in executive function in BDNF Val homozygotes, but CR was a nonsignificant predictor in BDNF Met carriers. APOE polymorphisms were not linked to the influence of CR on cognitive function. This result implicates BDNF in having an important role in capacity for building or accessing CR.
DOI: 10.1038/tp.2015.82
PubMed: 26125153
Links to Exploration step
pubmed:26125153Le document en format XML
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Ritchie</name><affiliation><nlm:affiliation>1] Neuroepidemiology of Ageing Research Unit, Imperial College, London, UK [2] Inserm, U1061 Neuropsychiatry, Montpellier, France.</nlm:affiliation></affiliation></author><author><name sortKey="Summers, J J" sort="Summers, J J" uniqKey="Summers J" first="J J" last="Summers">J J Summers</name><affiliation><nlm:affiliation>1] School of Medicine, University of Tasmania, Hobart, TAS, Australia [2] Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, UK.</nlm:affiliation></affiliation></author><author><name sortKey="Vickers, J C" sort="Vickers, J C" uniqKey="Vickers J" first="J C" last="Vickers">J C Vickers</name><affiliation><nlm:affiliation>1] School of Medicine, University of Tasmania, Hobart, TAS, Australia [2] Wicking Dementia Research and Education Centre, University of Tasmania, Hobart, TAS, Australia.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:26125153</idno><idno type="pmid">26125153</idno><idno type="doi">10.1038/tp.2015.82</idno><idno type="wicri:Area/PubMed/Corpus">002C40</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002C40</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The BDNF Val66Met polymorphism moderates the relationship between cognitive reserve and executive function.</title><author><name sortKey="Ward, D D" sort="Ward, D D" uniqKey="Ward D" first="D D" last="Ward">D D Ward</name><affiliation><nlm:affiliation>1] School of Medicine, University of Tasmania, Hobart, TAS, Australia [2] Wicking Dementia Research and Education Centre, University of Tasmania, Hobart, TAS, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Summers, M J" sort="Summers, M J" uniqKey="Summers M" first="M J" last="Summers">M J Summers</name><affiliation><nlm:affiliation>1] Wicking Dementia Research and Education Centre, University of Tasmania, Hobart, TAS, Australia [2] School of Social Sciences, University of the Sunshine Coast, Sippy Downs, QLD, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Saunders, N L" sort="Saunders, N L" uniqKey="Saunders N" first="N L" last="Saunders">N L Saunders</name><affiliation><nlm:affiliation>Wicking Dementia Research and Education Centre, University of Tasmania, Hobart, TAS, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Ritchie, K" sort="Ritchie, K" uniqKey="Ritchie K" first="K" last="Ritchie">K. Ritchie</name><affiliation><nlm:affiliation>1] Neuroepidemiology of Ageing Research Unit, Imperial College, London, UK [2] Inserm, U1061 Neuropsychiatry, Montpellier, France.</nlm:affiliation></affiliation></author><author><name sortKey="Summers, J J" sort="Summers, J J" uniqKey="Summers J" first="J J" last="Summers">J J Summers</name><affiliation><nlm:affiliation>1] School of Medicine, University of Tasmania, Hobart, TAS, Australia [2] Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, UK.</nlm:affiliation></affiliation></author><author><name sortKey="Vickers, J C" sort="Vickers, J C" uniqKey="Vickers J" first="J C" last="Vickers">J C Vickers</name><affiliation><nlm:affiliation>1] School of Medicine, University of Tasmania, Hobart, TAS, Australia [2] Wicking Dementia Research and Education Centre, University of Tasmania, Hobart, TAS, Australia.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Translational psychiatry</title><idno type="eISSN">2158-3188</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Apolipoproteins E (genetics)</term><term>Brain-Derived Neurotrophic Factor (genetics)</term><term>Cognition</term><term>Cognitive Reserve</term><term>Executive Function</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Polymorphism, Genetic</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Apolipoproteins E</term><term>Brain-Derived Neurotrophic Factor</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Cognition</term><term>Cognitive Reserve</term><term>Executive Function</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Polymorphism, Genetic</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The concept of cognitive reserve (CR) has been proposed to account for observed discrepancies between pathology and its clinical manifestation due to underlying differences in brain structure and function. In 433 healthy older adults participating in the Tasmanian Healthy Brain Project, we investigated whether common polymorphic variations in apolipoprotein E (APOE) or brain-derived neurotrophic factor (BDNF) influenced the association between CR contributors and cognitive function in older adults. We show that BDNF Val66Met moderates the association between CR and executive function. CR accounted for 8.5% of the variance in executive function in BDNF Val homozygotes, but CR was a nonsignificant predictor in BDNF Met carriers. APOE polymorphisms were not linked to the influence of CR on cognitive function. This result implicates BDNF in having an important role in capacity for building or accessing CR.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26125153</PMID><DateCreated><Year>2015</Year><Month>07</Month><Day>01</Day></DateCreated><DateCompleted><Year>2016</Year><Month>03</Month><Day>01</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2158-3188</ISSN><JournalIssue CitedMedium="Internet"><Volume>5</Volume><PubDate><Year>2015</Year><Month>Jun</Month><Day>30</Day></PubDate></JournalIssue><Title>Translational psychiatry</Title><ISOAbbreviation>Transl Psychiatry</ISOAbbreviation></Journal><ArticleTitle>The BDNF Val66Met polymorphism moderates the relationship between cognitive reserve and executive function.</ArticleTitle><Pagination><MedlinePgn>e590</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/tp.2015.82</ELocationID><Abstract><AbstractText>The concept of cognitive reserve (CR) has been proposed to account for observed discrepancies between pathology and its clinical manifestation due to underlying differences in brain structure and function. In 433 healthy older adults participating in the Tasmanian Healthy Brain Project, we investigated whether common polymorphic variations in apolipoprotein E (APOE) or brain-derived neurotrophic factor (BDNF) influenced the association between CR contributors and cognitive function in older adults. We show that BDNF Val66Met moderates the association between CR and executive function. CR accounted for 8.5% of the variance in executive function in BDNF Val homozygotes, but CR was a nonsignificant predictor in BDNF Met carriers. APOE polymorphisms were not linked to the influence of CR on cognitive function. This result implicates BDNF in having an important role in capacity for building or accessing CR.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ward</LastName><ForeName>D D</ForeName><Initials>DD</Initials><AffiliationInfo><Affiliation>1] School of Medicine, University of Tasmania, Hobart, TAS, Australia [2] Wicking Dementia Research and Education Centre, University of Tasmania, Hobart, TAS, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Summers</LastName><ForeName>M J</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>1] Wicking Dementia Research and Education Centre, University of Tasmania, Hobart, TAS, Australia [2] School of Social Sciences, University of the Sunshine Coast, Sippy Downs, QLD, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Saunders</LastName><ForeName>N L</ForeName><Initials>NL</Initials><AffiliationInfo><Affiliation>Wicking Dementia Research and Education Centre, University of Tasmania, Hobart, TAS, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ritchie</LastName><ForeName>K</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>1] Neuroepidemiology of Ageing Research Unit, Imperial College, London, UK [2] Inserm, U1061 Neuropsychiatry, Montpellier, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Summers</LastName><ForeName>J J</ForeName><Initials>JJ</Initials><AffiliationInfo><Affiliation>1] School of Medicine, University of Tasmania, Hobart, TAS, Australia [2] Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vickers</LastName><ForeName>J C</ForeName><Initials>JC</Initials><AffiliationInfo><Affiliation>1] School of Medicine, University of Tasmania, Hobart, TAS, Australia [2] Wicking Dementia Research and Education Centre, University of Tasmania, Hobart, TAS, Australia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>06</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Transl Psychiatry</MedlineTA><NlmUniqueID>101562664</NlmUniqueID><ISSNLinking>2158-3188</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001057">Apolipoproteins E</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019208">Brain-Derived Neurotrophic Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C579455">brain-derived neurotrophic factor, 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