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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Sleep Modifies the Relation of <italic>APOE</italic> to the Risk of Alzheimer Disease and Neurofibrillary Tangle Pathology</title><author><name sortKey="Lim, Andrew S P" sort="Lim, Andrew S P" uniqKey="Lim A" first="Andrew S. P." last="Lim">Andrew S. P. Lim</name><affiliation><nlm:aff id="A1">Division of Neurology, Department of Medicine, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, Ontario, Canada; 2075 Bayview Avenue – M1-600; Toronto, ON M4N 3M5; Canada</nlm:aff></affiliation></author><author><name sortKey="Yu, Lei" sort="Yu, Lei" uniqKey="Yu L" first="Lei" last="Yu">Lei Yu</name><affiliation><nlm:aff id="A2">Rush Alzheimer’s Disease Center, Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois; 600 S. Paulina St. – Suite 1026; Chicago, IL 60612; United States of America</nlm:aff></affiliation></author><author><name sortKey="Kowgier, Matthew" sort="Kowgier, Matthew" uniqKey="Kowgier M" first="Matthew" last="Kowgier">Matthew Kowgier</name><affiliation><nlm:aff id="A3">Genetic Epidemiology and Biostatistics Platform, Ontario Institute for Cancer Research, University of Toronto, Toronto, Ontario, Canada; 101 College Street – Suite HL20, Toronto, Ontario M5G 1L7; Canada</nlm:aff></affiliation></author><author><name sortKey="Schneider, Julie A" sort="Schneider, Julie A" uniqKey="Schneider J" first="Julie A." last="Schneider">Julie A. Schneider</name><affiliation><nlm:aff id="A2">Rush Alzheimer’s Disease Center, Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois; 600 S. Paulina St. – Suite 1026; Chicago, IL 60612; United States of America</nlm:aff></affiliation></author><author><name sortKey="Buchman, Aron S" sort="Buchman, Aron S" uniqKey="Buchman A" first="Aron S." last="Buchman">Aron S. Buchman</name><affiliation><nlm:aff id="A2">Rush Alzheimer’s Disease Center, Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois; 600 S. Paulina St. – Suite 1026; Chicago, IL 60612; United States of America</nlm:aff></affiliation></author><author><name sortKey="Bennett, David A" sort="Bennett, David A" uniqKey="Bennett D" first="David A." last="Bennett">David A. Bennett</name><affiliation><nlm:aff id="A2">Rush Alzheimer’s Disease Center, Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois; 600 S. Paulina St. – Suite 1026; Chicago, IL 60612; United States of America</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">24145819</idno><idno type="pmc">3859706</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3859706</idno><idno type="RBID">PMC:3859706</idno><idno type="doi">10.1001/jamaneurol.2013.4215</idno><date when="2013">2013</date><idno type="wicri:Area/Pmc/Corpus">000771</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000771</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Sleep Modifies the Relation of <italic>APOE</italic> to the Risk of Alzheimer Disease and Neurofibrillary Tangle Pathology</title><author><name sortKey="Lim, Andrew S P" sort="Lim, Andrew S P" uniqKey="Lim A" first="Andrew S. P." last="Lim">Andrew S. P. Lim</name><affiliation><nlm:aff id="A1">Division of Neurology, Department of Medicine, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, Ontario, Canada; 2075 Bayview Avenue – M1-600; Toronto, ON M4N 3M5; Canada</nlm:aff></affiliation></author><author><name sortKey="Yu, Lei" sort="Yu, Lei" uniqKey="Yu L" first="Lei" last="Yu">Lei Yu</name><affiliation><nlm:aff id="A2">Rush Alzheimer’s Disease Center, Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois; 600 S. Paulina St. – Suite 1026; Chicago, IL 60612; United States of America</nlm:aff></affiliation></author><author><name sortKey="Kowgier, Matthew" sort="Kowgier, Matthew" uniqKey="Kowgier M" first="Matthew" last="Kowgier">Matthew Kowgier</name><affiliation><nlm:aff id="A3">Genetic Epidemiology and Biostatistics Platform, Ontario Institute for Cancer Research, University of Toronto, Toronto, Ontario, Canada; 101 College Street – Suite HL20, Toronto, Ontario M5G 1L7; Canada</nlm:aff></affiliation></author><author><name sortKey="Schneider, Julie A" sort="Schneider, Julie A" uniqKey="Schneider J" first="Julie A." last="Schneider">Julie A. Schneider</name><affiliation><nlm:aff id="A2">Rush Alzheimer’s Disease Center, Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois; 600 S. Paulina St. – Suite 1026; Chicago, IL 60612; United States of America</nlm:aff></affiliation></author><author><name sortKey="Buchman, Aron S" sort="Buchman, Aron S" uniqKey="Buchman A" first="Aron S." last="Buchman">Aron S. Buchman</name><affiliation><nlm:aff id="A2">Rush Alzheimer’s Disease Center, Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois; 600 S. Paulina St. – Suite 1026; Chicago, IL 60612; United States of America</nlm:aff></affiliation></author><author><name sortKey="Bennett, David A" sort="Bennett, David A" uniqKey="Bennett D" first="David A." last="Bennett">David A. Bennett</name><affiliation><nlm:aff id="A2">Rush Alzheimer’s Disease Center, Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois; 600 S. Paulina St. – Suite 1026; Chicago, IL 60612; United States of America</nlm:aff></affiliation></author></analytic><series><title level="j">JAMA neurology</title><idno type="ISSN">2168-6149</idno><idno type="eISSN">2168-6157</idno><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec id="S1"><title>IMPORTANCE</title><p id="P1">The Apolipoprotein E (<italic>APOE</italic>) ε4 allele is a common and well-established genetic risk factor for Alzheimer Disease (AD). Sleep consolidation is also associated with AD risk and previous work suggests that <italic>APOE</italic> genotype and sleep may interact to influence cognitive function.</p></sec><sec id="S2"><title>OBJECTIVE</title><p id="P2">To determine whether better sleep consolidation attenuates the relation of the <italic>APOE</italic> genotype to the risk of incident AD and the burden of AD pathology.</p></sec><sec id="S3"><title>DESIGN</title><p id="P3">Prospective longitudinal cohort study with up to 6 years of follow-up.</p></sec><sec id="S4"><title>SETTING</title><p id="P4">Community-based.</p></sec><sec id="S5"><title>PARTICIPANTS</title><p id="P5">We studied a volunteer sample of 698 community dwelling older adults without dementia (average age 81.7 years; 77% female) in the Rush Memory and Aging Project followed for up to 6 years.</p></sec><sec id="S6"><title>EXPOSURES</title><p id="P6">We used up to 10 days of actigraphic recording to quantify the degree of sleep consolidation, and ascertained <italic>APOE</italic> genotype.</p></sec><sec id="S7"><title>MAIN OUTCOME MEASURES</title><p id="P7">Subjects underwent annual evaluation for AD over a follow-up period of up to 6 years. Autopsies were performed on 201 deceased participants, and Aβ and neurofibrillary tangle (NFT) pathology were identified by immunohistochemistry and quantified.</p></sec><sec id="S8"><title>RESULTS</title><p id="P8">Over a follow-up period, 98 individuals developed AD. In a series of Cox proportional hazards models, better sleep consolidation attenuated the effect of the ε4 allele on the risk of incident AD (HR 0.67 95%CI 0.46–0.97 p=0.036 per allele per 1SD increase in sleep consolidation). In a series of linear mixed effect models, better sleep consolidation also attenuated the effect of the ε4 allele on the annual rate of cognitive decline (interaction estimate +0.048 SE=0.012 p<0.001). In deceased individuals, better sleep consolidation attenuated the effect of the ε4 allele on NFT density (interaction estimate −0.42 SE=0.17 p=0.016), which accounted for the effect of sleep consolidation on the association between <italic>APOE</italic> genotype and cognition proximate to death.</p></sec><sec id="S9"><title>CONCLUSIONS AND RELEVANCE</title><p id="P9">Better sleep consolidation attenuates the effect of <italic>APOE</italic> genotype on incident AD and NFT pathology. Assessment of sleep consolidation may identify <italic>APOE</italic> positive individuals at high risk for incident AD, and interventions to enhance sleep consolidation should be studied as potentially useful means to reduce the risk of AD and NFT pathology in <italic>APOE</italic> ε4<sup>+</sup> individuals.</p></sec></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">101589536</journal-id><journal-id journal-id-type="pubmed-jr-id">40865</journal-id><journal-id journal-id-type="nlm-ta">JAMA Neurol</journal-id><journal-id journal-id-type="iso-abbrev">JAMA Neurol</journal-id><journal-title-group><journal-title>JAMA neurology</journal-title></journal-title-group><issn pub-type="ppub">2168-6149</issn><issn pub-type="epub">2168-6157</issn></journal-meta><article-meta><article-id pub-id-type="pmid">24145819</article-id><article-id pub-id-type="pmc">3859706</article-id><article-id pub-id-type="doi">10.1001/jamaneurol.2013.4215</article-id><article-id pub-id-type="manuscript">NIHMS509303</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Sleep Modifies the Relation of <italic>APOE</italic> to the Risk of Alzheimer Disease and Neurofibrillary Tangle Pathology</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Lim</surname><given-names>Andrew S.P.</given-names></name><degrees>MD</degrees><xref ref-type="aff" rid="A1">[1]</xref><email>andrew.lim@utoronto.ca</email></contrib><contrib contrib-type="author"><name><surname>Yu</surname><given-names>Lei</given-names></name><degrees>PhD</degrees><xref ref-type="aff" rid="A2">[2]</xref><email>lei_yu@rush.edu</email></contrib><contrib contrib-type="author"><name><surname>Kowgier</surname><given-names>Matthew</given-names></name><degrees>PhD</degrees><xref ref-type="aff" rid="A3">[3]</xref><email>matthew.kowgier@oicr.on.ca</email></contrib><contrib contrib-type="author"><name><surname>Schneider</surname><given-names>Julie A.</given-names></name><degrees>MD</degrees><xref ref-type="aff" rid="A2">[2]</xref><email>julie_a_schneider@rush.edu</email></contrib><contrib contrib-type="author"><name><surname>Buchman</surname><given-names>Aron S.</given-names></name><degrees>MD</degrees><xref ref-type="aff" rid="A2">[2]</xref><email>aron_s_buchman@rush.edu</email></contrib><contrib contrib-type="author"><name><surname>Bennett</surname><given-names>David A.</given-names></name><degrees>MD</degrees><xref ref-type="aff" rid="A2">[2]</xref><email>david_a_bennett@rush.edu</email></contrib></contrib-group><aff id="A1"><label>[1]</label>Division of Neurology, Department of Medicine, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, Ontario, Canada; 2075 Bayview Avenue – M1-600; Toronto, ON M4N 3M5; Canada</aff><aff id="A2"><label>[2]</label>Rush Alzheimer’s Disease Center, Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois; 600 S. Paulina St. – Suite 1026; Chicago, IL 60612; United States of America</aff><aff id="A3"><label>[3]</label>Genetic Epidemiology and Biostatistics Platform, Ontario Institute for Cancer Research, University of Toronto, Toronto, Ontario, Canada; 101 College Street – Suite HL20, Toronto, Ontario M5G 1L7; Canada</aff><author-notes><corresp id="FN1">Corresponding Author: Andrew S.P. Lim; Assistant Professor, Division of Neurology, Department of Medicine; Sunnybrook Health Sciences Centre; University of Toronto; 2075 Bayview Ave – M1600 Toronto, Ontario, Canada M4N 3M5 Phone: 416-480-6100 x2461 Fax: 416-480-6092 <email>andrew.lim@utoronto.ca</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>3</day><month>8</month><year>2013</year></pub-date><pub-date pub-type="ppub"><day>1</day><month>12</month><year>2013</year></pub-date><pub-date pub-type="pmc-release"><day>01</day><month>12</month><year>2014</year></pub-date><volume>70</volume><issue>12</issue><elocation-id>10.1001/jamaneurol.2013.4215</elocation-id><abstract><sec id="S1"><title>IMPORTANCE</title><p id="P1">The Apolipoprotein E (<italic>APOE</italic>) ε4 allele is a common and well-established genetic risk factor for Alzheimer Disease (AD). Sleep consolidation is also associated with AD risk and previous work suggests that <italic>APOE</italic> genotype and sleep may interact to influence cognitive function.</p></sec><sec id="S2"><title>OBJECTIVE</title><p id="P2">To determine whether better sleep consolidation attenuates the relation of the <italic>APOE</italic> genotype to the risk of incident AD and the burden of AD pathology.</p></sec><sec id="S3"><title>DESIGN</title><p id="P3">Prospective longitudinal cohort study with up to 6 years of follow-up.</p></sec><sec id="S4"><title>SETTING</title><p id="P4">Community-based.</p></sec><sec id="S5"><title>PARTICIPANTS</title><p id="P5">We studied a volunteer sample of 698 community dwelling older adults without dementia (average age 81.7 years; 77% female) in the Rush Memory and Aging Project followed for up to 6 years.</p></sec><sec id="S6"><title>EXPOSURES</title><p id="P6">We used up to 10 days of actigraphic recording to quantify the degree of sleep consolidation, and ascertained <italic>APOE</italic> genotype.</p></sec><sec id="S7"><title>MAIN OUTCOME MEASURES</title><p id="P7">Subjects underwent annual evaluation for AD over a follow-up period of up to 6 years. Autopsies were performed on 201 deceased participants, and Aβ and neurofibrillary tangle (NFT) pathology were identified by immunohistochemistry and quantified.</p></sec><sec id="S8"><title>RESULTS</title><p id="P8">Over a follow-up period, 98 individuals developed AD. In a series of Cox proportional hazards models, better sleep consolidation attenuated the effect of the ε4 allele on the risk of incident AD (HR 0.67 95%CI 0.46–0.97 p=0.036 per allele per 1SD increase in sleep consolidation). In a series of linear mixed effect models, better sleep consolidation also attenuated the effect of the ε4 allele on the annual rate of cognitive decline (interaction estimate +0.048 SE=0.012 p<0.001). In deceased individuals, better sleep consolidation attenuated the effect of the ε4 allele on NFT density (interaction estimate −0.42 SE=0.17 p=0.016), which accounted for the effect of sleep consolidation on the association between <italic>APOE</italic> genotype and cognition proximate to death.</p></sec><sec id="S9"><title>CONCLUSIONS AND RELEVANCE</title><p id="P9">Better sleep consolidation attenuates the effect of <italic>APOE</italic> genotype on incident AD and NFT pathology. Assessment of sleep consolidation may identify <italic>APOE</italic> positive individuals at high risk for incident AD, and interventions to enhance sleep consolidation should be studied as potentially useful means to reduce the risk of AD and NFT pathology in <italic>APOE</italic> ε4<sup>+</sup> individuals.</p></sec></abstract><funding-group><award-group><funding-source country="United States">National Institute of Neurological Disorders and Stroke : NINDS</funding-source><award-id>R01 NS078009 || NS</award-id></award-group><award-group><funding-source country="United States">National Institute on Aging : NIA</funding-source><award-id>R01 AG043379 || AG</award-id></award-group><award-group><funding-source country="United States">National Institute on Aging : NIA</funding-source><award-id>R01 AG042210 || AG</award-id></award-group><award-group><funding-source country="United States">National Institute on Aging : NIA</funding-source><award-id>R01 AG024480 || AG</award-id></award-group><award-group><funding-source country="United States">National Institute on Aging : NIA</funding-source><award-id>R01 AG017917 || AG</award-id></award-group><award-group><funding-source country="United States">National Institute on Aging : NIA</funding-source><award-id>R01 AG015819 || AG</award-id></award-group><award-group><funding-source country="United States">National Institute on Aging : NIA</funding-source><award-id>P30 AG010161 || AG</award-id></award-group><award-group><funding-source country="United States">National Institute on Aging : NIA</funding-source><award-id>P30 AG010161 || AG</award-id></award-group><award-group><funding-source country="United States">National Institute on Aging : NIA</funding-source><award-id>P01 AG009466 || AG</award-id></award-group><award-group><funding-source country="United States">National Institute on Aging : NIA</funding-source><award-id>K08 AG000849 || AG</award-id></award-group></funding-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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