Cognition and beta-amyloid in preclinical Alzheimer's disease: Data from the AIBL study
Identifieur interne : 004527 ( PascalFrancis/Curation ); précédent : 004526; suivant : 004528Cognition and beta-amyloid in preclinical Alzheimer's disease: Data from the AIBL study
Auteurs : Kerryn E. Pike [Australie] ; Kathryn A. Ellis [Australie] ; Victor L. Villemagne [Australie] ; Norm Good [Australie] ; Gael Chetelat [Australie, France] ; David Ames [Australie] ; Cassandra Szoeke [Australie] ; Simon M. Laws [Australie] ; Giuseppe Verdile [Australie] ; Ralph N. Martins [Australie] ; Colin L. Masters [Australie] ; Christopher C. Rowe [Australie]Source :
- Neuropsychologia [ 0028-3932 ] ; 2011.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme, Personne âgée.
English descriptors
- KwdEn :
Abstract
The 'preclinical' phase of Alzheimer's disease is a future target for treatment, but additional research is essential to understand the relationship between β-amyloid burden and cognition during this time. We investigated this relationship using a large sample of apparently healthy older adults (N= 177), which also enabled examination of whether the relationship differed according to age, gender, years of education, apolipoprotein E status, and the presence of subjective memory complaints. In addition to episodic memory, a range of cognitive measures (global cognition, semantic memory, visuospatial performance, and executive function) were examined. Participants were aged over 60 years with no objective cognitive impairment and came from the imaging arm of the Australian Imaging, Biomarkers, and Lifestyle (AIBL) study of ageing. 11C-PiB PET was used to measure β-amyloid burden and a PiB'cut-off' level of 1.5 was used to separate participants with low PiB retention from those with high PiB retention. Thirty-three percent of participants had a PiB positive scan. PiB positive participants were 5 years older, twice as likely to carry an apolipoprotein E ε4 allele, and their composite episodic memory was 0.26 SD worse than PiB negative volunteers. Linear regressions with β-amyloid burden as a dichotomous predictor, revealed an interaction between β-amyloid burden and gender, as well as age and education effects, in predicting episodic memory and visuospatial performance. In females, but not in males, increased β-amyloid was related to worse episodic memory and visuospatial performance. Furthermore, an interaction between β-amyloid burden and APOE status was found in predicting visuospatial performance, whereby there was a trend for increased β-amyloid to relate to worse visuospatial performance for those without an APOE ε4 allele. There were no other main or interaction effects of β-amyloid on any of the other composite cognitive measures. These cross-sectional findings suggest that β-amyloid burden does not have a large effect on cognition in this subset of apparently healthy older people. The finding of gender differences deserves further research to answer definitively the important question of gender susceptibility to adverse cognitive effects from β-amyloid.
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Cognition and beta-amyloid in preclinical Alzheimer's disease: Data from the AIBL study</title>
<author><name sortKey="Pike, Kerryn E" sort="Pike, Kerryn E" uniqKey="Pike K" first="Kerryn E." last="Pike">Kerryn E. Pike</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Nuclear Medicine, Centre for PET, Austin Health</s1>
<s2>Heidelberg, VIC</s2>
<s3>AUS</s3>
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<sZ>3 aut.</sZ>
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<affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Mental Health Research Institute</s1>
<s2>Parkville, VIC</s2>
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<affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Centre for Neurosciences, University of Melbourne</s1>
<s2>Parkville, VIC</s2>
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</affiliation>
<affiliation wicri:level="1"><inist:fA14 i1="04"><s1>School of Psychological Science, La Trobe University</s1>
<s2>Bundoora, VIC</s2>
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<sZ>1 aut.</sZ>
</inist:fA14>
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<author><name sortKey="Ellis, Kathryn A" sort="Ellis, Kathryn A" uniqKey="Ellis K" first="Kathryn A." last="Ellis">Kathryn A. Ellis</name>
<affiliation wicri:level="1"><inist:fA14 i1="05"><s1>Department of Psychiatry, University of Melbourne</s1>
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<author><name sortKey="Villemagne, Victor L" sort="Villemagne, Victor L" uniqKey="Villemagne V" first="Victor L." last="Villemagne">Victor L. Villemagne</name>
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<author><name sortKey="Good, Norm" sort="Good, Norm" uniqKey="Good N" first="Norm" last="Good">Norm Good</name>
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<author><name sortKey="Chetelat, Gael" sort="Chetelat, Gael" uniqKey="Chetelat G" first="Gael" last="Chetelat">Gael Chetelat</name>
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<author><name sortKey="Ames, David" sort="Ames, David" uniqKey="Ames D" first="David" last="Ames">David Ames</name>
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<author><name sortKey="Szoeke, Cassandra" sort="Szoeke, Cassandra" uniqKey="Szoeke C" first="Cassandra" last="Szoeke">Cassandra Szoeke</name>
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<author><name sortKey="Laws, Simon M" sort="Laws, Simon M" uniqKey="Laws S" first="Simon M." last="Laws">Simon M. Laws</name>
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<s2>Joondalup, Western Australia</s2>
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<s3>AUS</s3>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>10 aut.</sZ>
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<author><name sortKey="Verdile, Giuseppe" sort="Verdile, Giuseppe" uniqKey="Verdile G" first="Giuseppe" last="Verdile">Giuseppe Verdile</name>
<affiliation wicri:level="1"><inist:fA14 i1="10"><s1>Centre of Excellence for Alzheimer's Disease Research & Care, School of Exercise Biomedical and Health Sciences, Edith Cowan University</s1>
<s2>Joondalup, Western Australia</s2>
<s3>AUS</s3>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>10 aut.</sZ>
</inist:fA14>
<country>Australie</country>
</affiliation>
<affiliation wicri:level="1"><inist:fA14 i1="11"><s1>Sir James McCusker Alzheimer's Disease Research Unit (Hollywood Private Hospital)</s1>
<s2>Perth, Western Australia</s2>
<s3>AUS</s3>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>10 aut.</sZ>
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<author><name sortKey="Martins, Ralph N" sort="Martins, Ralph N" uniqKey="Martins R" first="Ralph N." last="Martins">Ralph N. Martins</name>
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<s2>Joondalup, Western Australia</s2>
<s3>AUS</s3>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>10 aut.</sZ>
</inist:fA14>
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</affiliation>
<affiliation wicri:level="1"><inist:fA14 i1="11"><s1>Sir James McCusker Alzheimer's Disease Research Unit (Hollywood Private Hospital)</s1>
<s2>Perth, Western Australia</s2>
<s3>AUS</s3>
<sZ>8 aut.</sZ>
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<author><name sortKey="Masters, Colin L" sort="Masters, Colin L" uniqKey="Masters C" first="Colin L." last="Masters">Colin L. Masters</name>
<affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Mental Health Research Institute</s1>
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<country>Australie</country>
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<affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Centre for Neurosciences, University of Melbourne</s1>
<s2>Parkville, VIC</s2>
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<author><name sortKey="Rowe, Christopher C" sort="Rowe, Christopher C" uniqKey="Rowe C" first="Christopher C." last="Rowe">Christopher C. Rowe</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Nuclear Medicine, Centre for PET, Austin Health</s1>
<s2>Heidelberg, VIC</s2>
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<country>Australie</country>
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<affiliation wicri:level="1"><inist:fA14 i1="12"><s1>Department of Medicine, University of Melbourne</s1>
<s2>Parkville, VIC</s2>
<s3>AUS</s3>
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<series><title level="j" type="main">Neuropsychologia</title>
<title level="j" type="abbreviated">Neuropsychologia</title>
<idno type="ISSN">0028-3932</idno>
<imprint><date when="2011">2011</date>
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<seriesStmt><title level="j" type="main">Neuropsychologia</title>
<title level="j" type="abbreviated">Neuropsychologia</title>
<idno type="ISSN">0028-3932</idno>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Ageing</term>
<term>Alzheimer disease</term>
<term>Cognition</term>
<term>Elderly</term>
<term>Emission tomography</term>
<term>Human</term>
<term>Medical imagery</term>
<term>Memory</term>
<term>Senescence</term>
<term>β Amyloid protein</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Cognition</term>
<term>Protéine amyloïde β</term>
<term>Démence d'Alzheimer</term>
<term>Mémoire</term>
<term>Sénescence</term>
<term>Vieillissement</term>
<term>Tomoscintigraphie</term>
<term>Imagerie médicale</term>
<term>Homme</term>
<term>Personne âgée</term>
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<front><div type="abstract" xml:lang="en">The 'preclinical' phase of Alzheimer's disease is a future target for treatment, but additional research is essential to understand the relationship between β-amyloid burden and cognition during this time. We investigated this relationship using a large sample of apparently healthy older adults (N<sub>=</sub>
177), which also enabled examination of whether the relationship differed according to age, gender, years of education, apolipoprotein E status, and the presence of subjective memory complaints. In addition to episodic memory, a range of cognitive measures (global cognition, semantic memory, visuospatial performance, and executive function) were examined. Participants were aged over 60 years with no objective cognitive impairment and came from the imaging arm of the Australian Imaging, Biomarkers, and Lifestyle (AIBL) study of ageing. <sup>11</sup>
C-PiB PET was used to measure β-amyloid burden and a PiB'cut-off' level of 1.5 was used to separate participants with low PiB retention from those with high PiB retention. Thirty-three percent of participants had a PiB positive scan. PiB positive participants were 5 years older, twice as likely to carry an apolipoprotein E ε4 allele, and their composite episodic memory was 0.26 SD worse than PiB negative volunteers. Linear regressions with β-amyloid burden as a dichotomous predictor, revealed an interaction between β-amyloid burden and gender, as well as age and education effects, in predicting episodic memory and visuospatial performance. In females, but not in males, increased β-amyloid was related to worse episodic memory and visuospatial performance. Furthermore, an interaction between β-amyloid burden and APOE status was found in predicting visuospatial performance, whereby there was a trend for increased β-amyloid to relate to worse visuospatial performance for those without an APOE ε4 allele. There were no other main or interaction effects of β-amyloid on any of the other composite cognitive measures. These cross-sectional findings suggest that β-amyloid burden does not have a large effect on cognition in this subset of apparently healthy older people. The finding of gender differences deserves further research to answer definitively the important question of gender susceptibility to adverse cognitive effects from β-amyloid.</div>
</front>
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<fA14 i1="07"><s1>Inserm-EPHE-Université de Caen/Basse-Normandie, Unite U923, GIP Cyceron, CHU Côte de Nacre</s1>
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<fA14 i1="10"><s1>Centre of Excellence for Alzheimer's Disease Research & Care, School of Exercise Biomedical and Health Sciences, Edith Cowan University</s1>
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<fA14 i1="11"><s1>Sir James McCusker Alzheimer's Disease Research Unit (Hollywood Private Hospital)</s1>
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C-PiB PET was used to measure β-amyloid burden and a PiB'cut-off' level of 1.5 was used to separate participants with low PiB retention from those with high PiB retention. Thirty-three percent of participants had a PiB positive scan. PiB positive participants were 5 years older, twice as likely to carry an apolipoprotein E ε4 allele, and their composite episodic memory was 0.26 SD worse than PiB negative volunteers. Linear regressions with β-amyloid burden as a dichotomous predictor, revealed an interaction between β-amyloid burden and gender, as well as age and education effects, in predicting episodic memory and visuospatial performance. In females, but not in males, increased β-amyloid was related to worse episodic memory and visuospatial performance. Furthermore, an interaction between β-amyloid burden and APOE status was found in predicting visuospatial performance, whereby there was a trend for increased β-amyloid to relate to worse visuospatial performance for those without an APOE ε4 allele. There were no other main or interaction effects of β-amyloid on any of the other composite cognitive measures. These cross-sectional findings suggest that β-amyloid burden does not have a large effect on cognition in this subset of apparently healthy older people. The finding of gender differences deserves further research to answer definitively the important question of gender susceptibility to adverse cognitive effects from β-amyloid.</s0>
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