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Cognition and beta-amyloid in preclinical Alzheimer's disease: Data from the AIBL study

Identifieur interne : 004527 ( PascalFrancis/Curation ); précédent : 004526; suivant : 004528

Cognition 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 :

RBID : Pascal:11-0384044

Descripteurs français

English descriptors

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.
pA  
A01 01  1    @0 0028-3932
A02 01      @0 NUPSA6
A03   1    @0 Neuropsychologia
A05       @2 49
A06       @2 9
A08 01  1  ENG  @1 Cognition and beta-amyloid in preclinical Alzheimer's disease: Data from the AIBL study
A11 01  1    @1 PIKE (Kerryn E.)
A11 02  1    @1 ELLIS (Kathryn A.)
A11 03  1    @1 VILLEMAGNE (Victor L.)
A11 04  1    @1 GOOD (Norm)
A11 05  1    @1 CHETELAT (Gael)
A11 06  1    @1 AMES (David)
A11 07  1    @1 SZOEKE (Cassandra)
A11 08  1    @1 LAWS (Simon M.)
A11 09  1    @1 VERDILE (Giuseppe)
A11 10  1    @1 MARTINS (Ralph N.)
A11 11  1    @1 MASTERS (Colin L.)
A11 12  1    @1 ROWE (Christopher C.)
A14 01      @1 Department of Nuclear Medicine, Centre for PET, Austin Health @2 Heidelberg, VIC @3 AUS @Z 1 aut. @Z 3 aut. @Z 5 aut. @Z 12 aut.
A14 02      @1 Mental Health Research Institute @2 Parkville, VIC @3 AUS @Z 1 aut. @Z 3 aut. @Z 11 aut.
A14 03      @1 Centre for Neurosciences, University of Melbourne @2 Parkville, VIC @3 AUS @Z 1 aut. @Z 3 aut. @Z 11 aut.
A14 04      @1 School of Psychological Science, La Trobe University @2 Bundoora, VIC @3 AUS @Z 1 aut.
A14 05      @1 Department of Psychiatry, University of Melbourne @2 Parkville, VIC @3 AUS @Z 2 aut. @Z 6 aut.
A14 06      @1 CSIRO Mathematics, Informatics and Statistics, Australian E-Health Research Centre @2 Herston, QLD @3 AUS @Z 4 aut.
A14 07      @1 Inserm-EPHE-Université de Caen/Basse-Normandie, Unite U923, GIP Cyceron, CHU Côte de Nacre @2 Caen @3 FRA @Z 5 aut.
A14 08      @1 National Ageing Research Institute @2 Parkville, VIC @3 AUS @Z 6 aut.
A14 09      @1 CSIRO Neurodegenerative Disease, Mental Disorders & Brain Health, Preventative Health Flagship, CSIRO Molecular and Health Technologies @2 Parkville, VIC @3 AUS @Z 7 aut.
A14 10      @1 Centre of Excellence for Alzheimer's Disease Research & Care, School of Exercise Biomedical and Health Sciences, Edith Cowan University @2 Joondalup, Western Australia @3 AUS @Z 8 aut. @Z 9 aut. @Z 10 aut.
A14 11      @1 Sir James McCusker Alzheimer's Disease Research Unit (Hollywood Private Hospital) @2 Perth, Western Australia @3 AUS @Z 8 aut. @Z 9 aut. @Z 10 aut.
A14 12      @1 Department of Medicine, University of Melbourne @2 Parkville, VIC @3 AUS @Z 12 aut.
A20       @1 2384-2390
A21       @1 2011
A23 01      @0 ENG
A43 01      @1 INIST @2 11143 @5 354000508504460110
A44       @0 0000 @1 © 2011 INIST-CNRS. All rights reserved.
A45       @0 1 p.1/4
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A60       @1 P
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A64 01  1    @0 Neuropsychologia
A66 01      @0 GBR
C01 01    ENG  @0 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.
C02 01  X    @0 002B18C13
C02 02  X    @0 002B17G
C03 01  X  FRE  @0 Cognition @5 01
C03 01  X  ENG  @0 Cognition @5 01
C03 01  X  SPA  @0 Cognición @5 01
C03 02  X  FRE  @0 Protéine amyloïde β @5 02
C03 02  X  ENG  @0 β Amyloid protein @5 02
C03 02  X  SPA  @0 Proteína amiloide β @5 02
C03 03  X  FRE  @0 Démence d'Alzheimer @5 03
C03 03  X  ENG  @0 Alzheimer disease @5 03
C03 03  X  SPA  @0 Demencia Alzheimer @5 03
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C03 06  X  SPA  @0 Envejecimiento @5 06
C03 07  X  FRE  @0 Tomoscintigraphie @5 07
C03 07  X  ENG  @0 Emission tomography @5 07
C03 07  X  SPA  @0 Tomocentelleografía @5 07
C03 08  X  FRE  @0 Imagerie médicale @5 08
C03 08  X  ENG  @0 Medical imagery @5 08
C03 08  X  SPA  @0 Imaginería médica @5 08
C03 09  X  FRE  @0 Homme @5 18
C03 09  X  ENG  @0 Human @5 18
C03 09  X  SPA  @0 Hombre @5 18
C03 10  X  FRE  @0 Personne âgée @5 19
C03 10  X  ENG  @0 Elderly @5 19
C03 10  X  SPA  @0 Anciano @5 19
C07 01  X  FRE  @0 Pathologie de l'encéphale @5 37
C07 01  X  ENG  @0 Cerebral disorder @5 37
C07 01  X  SPA  @0 Encéfalo patología @5 37
C07 02  X  FRE  @0 Maladie dégénérative @5 38
C07 02  X  ENG  @0 Degenerative disease @5 38
C07 02  X  SPA  @0 Enfermedad degenerativa @5 38
C07 03  X  FRE  @0 Pathologie du système nerveux central @5 39
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C07 04  X  ENG  @0 Nervous system diseases @5 40
C07 04  X  SPA  @0 Sistema nervioso patología @5 40
N21       @1 262

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Pascal:11-0384044

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<title xml:lang="en" level="a">Cognition and beta-amyloid in preclinical Alzheimer's disease: Data from the AIBL study</title>
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<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
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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>
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<s0>Ageing</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>Envejecimiento</s0>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE">
<s0>Tomoscintigraphie</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Emission tomography</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
<s0>Tomocentelleografía</s0>
<s5>07</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE">
<s0>Imagerie médicale</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
<s0>Medical imagery</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Imaginería médica</s0>
<s5>08</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE">
<s0>Homme</s0>
<s5>18</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG">
<s0>Human</s0>
<s5>18</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA">
<s0>Hombre</s0>
<s5>18</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE">
<s0>Personne âgée</s0>
<s5>19</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG">
<s0>Elderly</s0>
<s5>19</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA">
<s0>Anciano</s0>
<s5>19</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Pathologie de l'encéphale</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Pathologie du système nerveux central</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Pathologie du système nerveux</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>40</s5>
</fC07>
<fN21>
<s1>262</s1>
</fN21>
</pA>
</standard>
</inist>
</record>

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