Regional amyloid burden and intrinsic connectivity networks in cognitively normal elderly subjects.
Identifieur interne : 000F09 ( PubMed/Corpus ); précédent : 000F08; suivant : 000F10Regional amyloid burden and intrinsic connectivity networks in cognitively normal elderly subjects.
Auteurs : Hyun Kook Lim ; Robert Nebes ; Beth Snitz ; Ann Cohen ; Chester Mathis ; Julie Price ; Lisa Weissfeld ; William Klunk ; Howard J. AizensteinSource :
- Brain : a journal of neurology [ 1460-2156 ] ; 2014.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Alzheimer Disease (metabolism), Alzheimer Disease (pathology), Amyloid (metabolism), Brain (metabolism), Brain (pathology), Brain Mapping (methods), Female, Humans, Image Processing, Computer-Assisted, Magnetic Resonance Imaging (methods), Male, Middle Aged, Nerve Net (physiopathology), Neuropsychological Tests.
- MESH :
- chemical , metabolism : Amyloid.
- metabolism : Alzheimer Disease, Brain.
- methods : Brain Mapping, Magnetic Resonance Imaging.
- pathology : Alzheimer Disease, Brain.
- physiopathology : Nerve Net.
- Aged, Aged, 80 and over, Female, Humans, Image Processing, Computer-Assisted, Male, Middle Aged, Neuropsychological Tests.
Abstract
Although previous studies demonstrated decreased functional connectivity in the default mode network in the cognitively normal older adults with amyloid burden, effects of amyloid burden in the other large-scale intrinsic connectivity networks are not yet clear. The aim of this study was to investigate the distinctive association pattern of amyloid-β deposition on the three large-scale intrinsic connectivity networks (the default mode network, salience network and central executive network) in older adults with normal cognition. Fifty-six older adults with normal cognition underwent functional magnetic resonance imaging and were dichotomized using 11C-labelled Pittsburgh compound B positron emission tomography imaging into subjects with (PiB+; n=27) and without (PiB-; n=29) detectable amyloid burden. We found that the functional connectivities of (i) the default mode network were greater; (ii) the salience network were not different; and (iii) the central executive network were lower in the Pittsburgh compound B positive group, compared with the Pittsburgh compound B negative group. Anterior cingulate cortex Pittsburgh compound B retention was negatively correlated with the functional connectivities of the posterior default mode network, and positively correlated with fronto-parietal functional connectivity (within the central executive network) in the Pittsburgh compound B positive group. The anti-correlation strength between the default mode network and the central executive network was negatively correlated with the anterior cingulate cortex Pittsburgh compound B levels. Additionally, significant group × episodic memory interactions with functional connectivities in the posterior default mode network, and the frontal default mode network were observed. Our results of aberrant default mode network functional connectivity and distinctive correlation patterns between the Pittsburgh compound B retention in the anterior cingulate cortex and functional connectivities in the default mode network and central executive network in the Pittsburgh compound B positive group might reflect a detrimental effect of amyloid retention on functional changes in the course of Alzheimer's disease progression.
DOI: 10.1093/brain/awu271
PubMed: 25266592
Links to Exploration step
pubmed:25266592Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Regional amyloid burden and intrinsic connectivity networks in cognitively normal elderly subjects.</title><author><name sortKey="Lim, Hyun Kook" sort="Lim, Hyun Kook" uniqKey="Lim H" first="Hyun Kook" last="Lim">Hyun Kook Lim</name><affiliation><nlm:affiliation>1 Department of Psychiatry, The Saint Vincent Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea 2 Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Nebes, Robert" sort="Nebes, Robert" uniqKey="Nebes R" first="Robert" last="Nebes">Robert Nebes</name><affiliation><nlm:affiliation>2 Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Snitz, Beth" sort="Snitz, Beth" uniqKey="Snitz B" first="Beth" last="Snitz">Beth Snitz</name><affiliation><nlm:affiliation>3 Department of Neurology, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Cohen, Ann" sort="Cohen, Ann" uniqKey="Cohen A" first="Ann" last="Cohen">Ann Cohen</name><affiliation><nlm:affiliation>2 Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Mathis, Chester" sort="Mathis, Chester" uniqKey="Mathis C" first="Chester" last="Mathis">Chester Mathis</name><affiliation><nlm:affiliation>4 Department of Radiology, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Price, Julie" sort="Price, Julie" uniqKey="Price J" first="Julie" last="Price">Julie Price</name><affiliation><nlm:affiliation>4 Department of Radiology, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Weissfeld, Lisa" sort="Weissfeld, Lisa" uniqKey="Weissfeld L" first="Lisa" last="Weissfeld">Lisa Weissfeld</name><affiliation><nlm:affiliation>5 Department of Biostatistics University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Klunk, William" sort="Klunk, William" uniqKey="Klunk W" first="William" last="Klunk">William Klunk</name><affiliation><nlm:affiliation>2 Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA 3 Department of Neurology, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Aizenstein, Howard J" sort="Aizenstein, Howard J" uniqKey="Aizenstein H" first="Howard J" last="Aizenstein">Howard J. Aizenstein</name><affiliation><nlm:affiliation>2 Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA haizenstein@gmail.com.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:25266592</idno><idno type="pmid">25266592</idno><idno type="doi">10.1093/brain/awu271</idno><idno type="wicri:Area/PubMed/Corpus">000F09</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000F09</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Regional amyloid burden and intrinsic connectivity networks in cognitively normal elderly subjects.</title><author><name sortKey="Lim, Hyun Kook" sort="Lim, Hyun Kook" uniqKey="Lim H" first="Hyun Kook" last="Lim">Hyun Kook Lim</name><affiliation><nlm:affiliation>1 Department of Psychiatry, The Saint Vincent Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea 2 Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Nebes, Robert" sort="Nebes, Robert" uniqKey="Nebes R" first="Robert" last="Nebes">Robert Nebes</name><affiliation><nlm:affiliation>2 Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Snitz, Beth" sort="Snitz, Beth" uniqKey="Snitz B" first="Beth" last="Snitz">Beth Snitz</name><affiliation><nlm:affiliation>3 Department of Neurology, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Cohen, Ann" sort="Cohen, Ann" uniqKey="Cohen A" first="Ann" last="Cohen">Ann Cohen</name><affiliation><nlm:affiliation>2 Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Mathis, Chester" sort="Mathis, Chester" uniqKey="Mathis C" first="Chester" last="Mathis">Chester Mathis</name><affiliation><nlm:affiliation>4 Department of Radiology, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Price, Julie" sort="Price, Julie" uniqKey="Price J" first="Julie" last="Price">Julie Price</name><affiliation><nlm:affiliation>4 Department of Radiology, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Weissfeld, Lisa" sort="Weissfeld, Lisa" uniqKey="Weissfeld L" first="Lisa" last="Weissfeld">Lisa Weissfeld</name><affiliation><nlm:affiliation>5 Department of Biostatistics University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Klunk, William" sort="Klunk, William" uniqKey="Klunk W" first="William" last="Klunk">William Klunk</name><affiliation><nlm:affiliation>2 Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA 3 Department of Neurology, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Aizenstein, Howard J" sort="Aizenstein, Howard J" uniqKey="Aizenstein H" first="Howard J" last="Aizenstein">Howard J. Aizenstein</name><affiliation><nlm:affiliation>2 Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA haizenstein@gmail.com.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Brain : a journal of neurology</title><idno type="eISSN">1460-2156</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Alzheimer Disease (metabolism)</term><term>Alzheimer Disease (pathology)</term><term>Amyloid (metabolism)</term><term>Brain (metabolism)</term><term>Brain (pathology)</term><term>Brain Mapping (methods)</term><term>Female</term><term>Humans</term><term>Image Processing, Computer-Assisted</term><term>Magnetic Resonance Imaging (methods)</term><term>Male</term><term>Middle Aged</term><term>Nerve Net (physiopathology)</term><term>Neuropsychological Tests</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Amyloid</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Alzheimer Disease</term><term>Brain</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Brain Mapping</term><term>Magnetic Resonance Imaging</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Alzheimer Disease</term><term>Brain</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Nerve Net</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Humans</term><term>Image Processing, Computer-Assisted</term><term>Male</term><term>Middle Aged</term><term>Neuropsychological Tests</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Although previous studies demonstrated decreased functional connectivity in the default mode network in the cognitively normal older adults with amyloid burden, effects of amyloid burden in the other large-scale intrinsic connectivity networks are not yet clear. The aim of this study was to investigate the distinctive association pattern of amyloid-β deposition on the three large-scale intrinsic connectivity networks (the default mode network, salience network and central executive network) in older adults with normal cognition. Fifty-six older adults with normal cognition underwent functional magnetic resonance imaging and were dichotomized using 11C-labelled Pittsburgh compound B positron emission tomography imaging into subjects with (PiB+; n=27) and without (PiB-; n=29) detectable amyloid burden. We found that the functional connectivities of (i) the default mode network were greater; (ii) the salience network were not different; and (iii) the central executive network were lower in the Pittsburgh compound B positive group, compared with the Pittsburgh compound B negative group. Anterior cingulate cortex Pittsburgh compound B retention was negatively correlated with the functional connectivities of the posterior default mode network, and positively correlated with fronto-parietal functional connectivity (within the central executive network) in the Pittsburgh compound B positive group. The anti-correlation strength between the default mode network and the central executive network was negatively correlated with the anterior cingulate cortex Pittsburgh compound B levels. Additionally, significant group × episodic memory interactions with functional connectivities in the posterior default mode network, and the frontal default mode network were observed. Our results of aberrant default mode network functional connectivity and distinctive correlation patterns between the Pittsburgh compound B retention in the anterior cingulate cortex and functional connectivities in the default mode network and central executive network in the Pittsburgh compound B positive group might reflect a detrimental effect of amyloid retention on functional changes in the course of Alzheimer's disease progression.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25266592</PMID><DateCreated><Year>2014</Year><Month>11</Month><Day>21</Day></DateCreated><DateCompleted><Year>2015</Year><Month>03</Month><Day>18</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1460-2156</ISSN><JournalIssue CitedMedium="Internet"><Volume>137</Volume><Issue>Pt 12</Issue><PubDate><Year>2014</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Brain : a journal of neurology</Title><ISOAbbreviation>Brain</ISOAbbreviation></Journal><ArticleTitle>Regional amyloid burden and intrinsic connectivity networks in cognitively normal elderly subjects.</ArticleTitle><Pagination><MedlinePgn>3327-38</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1093/brain/awu271</ELocationID><Abstract><AbstractText>Although previous studies demonstrated decreased functional connectivity in the default mode network in the cognitively normal older adults with amyloid burden, effects of amyloid burden in the other large-scale intrinsic connectivity networks are not yet clear. The aim of this study was to investigate the distinctive association pattern of amyloid-β deposition on the three large-scale intrinsic connectivity networks (the default mode network, salience network and central executive network) in older adults with normal cognition. Fifty-six older adults with normal cognition underwent functional magnetic resonance imaging and were dichotomized using 11C-labelled Pittsburgh compound B positron emission tomography imaging into subjects with (PiB+; n=27) and without (PiB-; n=29) detectable amyloid burden. We found that the functional connectivities of (i) the default mode network were greater; (ii) the salience network were not different; and (iii) the central executive network were lower in the Pittsburgh compound B positive group, compared with the Pittsburgh compound B negative group. Anterior cingulate cortex Pittsburgh compound B retention was negatively correlated with the functional connectivities of the posterior default mode network, and positively correlated with fronto-parietal functional connectivity (within the central executive network) in the Pittsburgh compound B positive group. The anti-correlation strength between the default mode network and the central executive network was negatively correlated with the anterior cingulate cortex Pittsburgh compound B levels. Additionally, significant group × episodic memory interactions with functional connectivities in the posterior default mode network, and the frontal default mode network were observed. Our results of aberrant default mode network functional connectivity and distinctive correlation patterns between the Pittsburgh compound B retention in the anterior cingulate cortex and functional connectivities in the default mode network and central executive network in the Pittsburgh compound B positive group might reflect a detrimental effect of amyloid retention on functional changes in the course of Alzheimer's disease progression.</AbstractText><CopyrightInformation>© The Author (2014). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.com.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lim</LastName><ForeName>Hyun Kook</ForeName><Initials>HK</Initials><AffiliationInfo><Affiliation>1 Department of Psychiatry, The Saint Vincent Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea 2 Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nebes</LastName><ForeName>Robert</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>2 Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Snitz</LastName><ForeName>Beth</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>3 Department of Neurology, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cohen</LastName><ForeName>Ann</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>2 Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mathis</LastName><ForeName>Chester</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>4 Department of Radiology, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Price</LastName><ForeName>Julie</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>4 Department of Radiology, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Weissfeld</LastName><ForeName>Lisa</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>5 Department of Biostatistics University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Klunk</LastName><ForeName>William</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>2 Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA 3 Department of Neurology, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aizenstein</LastName><ForeName>Howard J</ForeName><Initials>HJ</Initials><AffiliationInfo><Affiliation>2 Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA haizenstein@gmail.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>5K23AG038479</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 NS060184</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R37 AG025516</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 MH076079</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50 AG005133</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>RF1 AG025516</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 AG025204</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>09</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Brain</MedlineTA><NlmUniqueID>0372537</NlmUniqueID><ISSNLinking>0006-8950</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000682">Amyloid</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Nat Rev Neurol. 2014 Nov;10(11):609</RefSource><PMID Version="1">25330722</PMID></CommentsCorrections><CommentsCorrections RefType="CommentIn"><RefSource>Brain. 2014 Dec;137(Pt 12):3104-6</RefSource><PMID Version="1">25413934</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuron. 2009 Jul 30;63(2):178-88</RefSource><PMID Version="1">19640477</PMID></CommentsCorrections><CommentsCorrections 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