Regional dynamics of amyloid-β deposition in healthy elderly, mild cognitive impairment and Alzheimer's disease: a voxelwise PiB-PET longitudinal study
Identifieur interne : 001255 ( PascalFrancis/Corpus ); précédent : 001254; suivant : 001256Regional dynamics of amyloid-β deposition in healthy elderly, mild cognitive impairment and Alzheimer's disease: a voxelwise PiB-PET longitudinal study
Auteurs : Nicolas Villain ; Gaël Chetelat ; Blandine Grassiot ; Pierrick Bourgeat ; Gareth Jones ; Kathryn A. Ellis ; David Ames ; Ralph N. Martins ; Francis Eustache ; Olivier Salvado ; Colin L. Masters ; Christopher C. Rowe ; Victor L. VillemagneSource :
- Brain [ 0006-8950 ] ; 2012.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Amyloid-β deposition in Alzheimer's disease is thought to start while individuals are still cognitively unimpaired and it is hypothesized that after an early phase of fast accumulation, a plateau is reached by the time of cognitive decline. However, few longitudinal Pittsburgh compound B-positron emission tomography studies have tested this hypothesis, and with conflicting results. The purpose of this work is to further our understanding of the dynamics of amyloid-β deposition in a large longitudinal cohort. A total of 32 patients with Alzheimer's disease, 49 subjects with mild cognitive impairment and 103 healthy controls underwent two Pittsburgh compound B-positron emission tomography scans 18 months apart. For each participant, a parametric map of Pittsburgh compound B-positron emission tomography rate of change was created [(follow-up scan - baseline scan)/ follow-up duration] and entered in a voxelwise three-way analysis of covariance, with clinical status (healthy controls, mild cognitive impairment or Alzheimer's disease), disease progression (clinical conversion from healthy controls to mild cognitive impairment or Alzheimer's disease, or from mild cognitive impairment to Alzheimer's disease) and Pittsburgh compound B status (positive versus negative) as independent factors. Only a significant effect of the Pittsburgh compound B status was found: both Pittsburgh compound B-positive and -negative subjects showed a significant increase in amyloid-β deposition, with this increase being significantly higher in Pittsburgh compound B-positive individuals. This finding suggests either that Pittsburgh compound B-negative individuals have slower rates of amyloid-β accumulation than positive, or that the proportion of individuals showing significant increase in amyloid-β deposition, termed 'Pittsburgh compound B accumulators', is higher within the Pittsburgh compound B-positive group than within the Pittsburgh compound B-negative group. The bimodal distribution of the individual rates of neocortical amyloid-β accumulation observed support the existence of 'Pittsburgh compound B non-accumulators' and 'Pittsburgh compound B accumulators' and different clustering analyses led to a consistent threshold to separate these two subgroups (0.014-0.022 standardized uptake value ratiopons/year). The voxelwise three-way analysis of covariance was thus recomputed with the 'Pittsburgh compound B accumulators' only and the results were almost unchanged, with the Pittsburgh compound B-positive group showing higher accumulation than the Pittsburgh compound B-negative group. Finally, a significant negative correlation was found between Pittsburgh compound B rate of change and Pittsburgh compound B baseline burden, but only in the Pittsburgh compound B-positive group (r= -0.24; P=0.025). Higher rates of amyloid-β deposition are associated with higher amyloid-β burden suggesting that amyloid-β deposition does not reach a plateau when cognitive impairments manifest but is instead an ongoing process present even at the Alzheimer's disease stage. amyloid-β accumulation also seems to slow down at the latest stages of the process, i.e. in participants with the highest amyloid burden. Furthermore, this study identified the existence of Pittsburgh compound 'accumulators' and 'non-accumulators', notably within the Pittsburgh compound B-negative group, which may be a relevant concept for future studies.
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NO : | PASCAL 12-0279742 INIST |
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ET : | Regional dynamics of amyloid-β deposition in healthy elderly, mild cognitive impairment and Alzheimer's disease: a voxelwise PiB-PET longitudinal study |
AU : | VILLAIN (Nicolas); CHETELAT (Gaël); GRASSIOT (Blandine); BOURGEAT (Pierrick); JONES (Gareth); ELLIS (Kathryn A.); AMES (David); MARTINS (Ralph N.); EUSTACHE (Francis); SALVADO (Olivier); MASTERS (Colin L.); ROWE (Christopher C.); VILLEMAGNE (Victor L.) |
AF : | INSERM, U1077/Caen 14000/France (1 aut., 2 aut., 3 aut., 9 aut.); Université de Caen Basse-Normandie, UMR-S1077/Caen 14000/France (1 aut., 2 aut., 3 aut., 9 aut.); Ecole Pratique des Hautes Etudes, UMR-S1077/Caen 14000/France (1 aut., 2 aut., 3 aut., 9 aut.); CHU de Caen, U1077/Caen 14000/France (1 aut., 2 aut., 3 aut., 9 aut.); Department of Nuclear Medicine and Centre for PET, Austin Health, 145 Studley Road/Heidelberg, VIC 3084/Australie (2 aut., 5 aut., 12 aut., 13 aut.); CSIRO Preventative Health National Research Flagship ICTC, The Australian e-Health Research Centre, BioMedIA, Royal Brisbane and Women's Hospital/Herston, QLD 4006/Australie (4 aut., 10 aut.); Department of Psychiatry, University of Melbourne/Parkville, VIC 3052/Australie (6 aut., 7 aut.); Centre of Excellence for Alzheimer's Disease Research and Care, School of Exercise Biomedical and Health Sciences, Edith Cowan University/Joondalup, WA 6027/Australie (8 aut.); The Mental Health Research Institute, University of Melbourne/VIC 3000/Australie (6 aut., 11 aut., 13 aut.); Department of Medicine, Austin Health, University of Melbourne/VIC 3000/Australie (12 aut., 13 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Brain; ISSN 0006-8950; Royaume-Uni; Da. 2012; Vol. 135; No. p. 7; Pp. 2126-2139; Bibl. 1 p.1/4 |
LA : | Anglais |
EA : | Amyloid-β deposition in Alzheimer's disease is thought to start while individuals are still cognitively unimpaired and it is hypothesized that after an early phase of fast accumulation, a plateau is reached by the time of cognitive decline. However, few longitudinal Pittsburgh compound B-positron emission tomography studies have tested this hypothesis, and with conflicting results. The purpose of this work is to further our understanding of the dynamics of amyloid-β deposition in a large longitudinal cohort. A total of 32 patients with Alzheimer's disease, 49 subjects with mild cognitive impairment and 103 healthy controls underwent two Pittsburgh compound B-positron emission tomography scans 18 months apart. For each participant, a parametric map of Pittsburgh compound B-positron emission tomography rate of change was created [(follow-up scan - baseline scan)/ follow-up duration] and entered in a voxelwise three-way analysis of covariance, with clinical status (healthy controls, mild cognitive impairment or Alzheimer's disease), disease progression (clinical conversion from healthy controls to mild cognitive impairment or Alzheimer's disease, or from mild cognitive impairment to Alzheimer's disease) and Pittsburgh compound B status (positive versus negative) as independent factors. Only a significant effect of the Pittsburgh compound B status was found: both Pittsburgh compound B-positive and -negative subjects showed a significant increase in amyloid-β deposition, with this increase being significantly higher in Pittsburgh compound B-positive individuals. This finding suggests either that Pittsburgh compound B-negative individuals have slower rates of amyloid-β accumulation than positive, or that the proportion of individuals showing significant increase in amyloid-β deposition, termed 'Pittsburgh compound B accumulators', is higher within the Pittsburgh compound B-positive group than within the Pittsburgh compound B-negative group. The bimodal distribution of the individual rates of neocortical amyloid-β accumulation observed support the existence of 'Pittsburgh compound B non-accumulators' and 'Pittsburgh compound B accumulators' and different clustering analyses led to a consistent threshold to separate these two subgroups (0.014-0.022 standardized uptake value ratiopons/year). The voxelwise three-way analysis of covariance was thus recomputed with the 'Pittsburgh compound B accumulators' only and the results were almost unchanged, with the Pittsburgh compound B-positive group showing higher accumulation than the Pittsburgh compound B-negative group. Finally, a significant negative correlation was found between Pittsburgh compound B rate of change and Pittsburgh compound B baseline burden, but only in the Pittsburgh compound B-positive group (r= -0.24; P=0.025). Higher rates of amyloid-β deposition are associated with higher amyloid-β burden suggesting that amyloid-β deposition does not reach a plateau when cognitive impairments manifest but is instead an ongoing process present even at the Alzheimer's disease stage. amyloid-β accumulation also seems to slow down at the latest stages of the process, i.e. in participants with the highest amyloid burden. Furthermore, this study identified the existence of Pittsburgh compound 'accumulators' and 'non-accumulators', notably within the Pittsburgh compound B-negative group, which may be a relevant concept for future studies. |
CC : | 002B17; 002B17G |
FD : | Déficit cognitif léger; Trouble cognitif; Démence d'Alzheimer; Pathologie du système nerveux; Amyloïde; Personne âgée; Tomoscintigraphie; Tomographie par émission de positons; Vieillissement |
FG : | Homme; Pathologie de l'encéphale; Maladie dégénérative; Pathologie du système nerveux central |
ED : | mild cognitive impairment; Cognitive disorder; Alzheimer disease; Nervous system diseases; Amyloid; Elderly; Emission tomography; Positron emission tomography; Ageing |
EG : | Human; Cerebral disorder; Degenerative disease; Central nervous system disease |
SD : | Disturbio cognitivo ligero; Trastorno cognitivo; Demencia Alzheimer; Sistema nervioso patología; Amiloide; Anciano; Tomocentelleografía; Tomografía emisión positrones; Envejecimiento |
LO : | INIST-998.354000505272590120 |
ID : | 12-0279742 |
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Pascal:12-0279742Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Regional dynamics of amyloid-β deposition in healthy elderly, mild cognitive impairment and Alzheimer's disease: a voxelwise PiB-PET longitudinal study</title>
<author><name sortKey="Villain, Nicolas" sort="Villain, Nicolas" uniqKey="Villain N" first="Nicolas" last="Villain">Nicolas Villain</name>
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<series><title level="j" type="main">Brain</title>
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<idno type="ISSN">0006-8950</idno>
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<term>Alzheimer disease</term>
<term>Amyloid</term>
<term>Cognitive disorder</term>
<term>Elderly</term>
<term>Emission tomography</term>
<term>Nervous system diseases</term>
<term>Positron emission tomography</term>
<term>mild cognitive impairment</term>
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<term>Trouble cognitif</term>
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<term>Pathologie du système nerveux</term>
<term>Amyloïde</term>
<term>Personne âgée</term>
<term>Tomoscintigraphie</term>
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<front><div type="abstract" xml:lang="en">Amyloid-β deposition in Alzheimer's disease is thought to start while individuals are still cognitively unimpaired and it is hypothesized that after an early phase of fast accumulation, a plateau is reached by the time of cognitive decline. However, few longitudinal Pittsburgh compound B-positron emission tomography studies have tested this hypothesis, and with conflicting results. The purpose of this work is to further our understanding of the dynamics of amyloid-β deposition in a large longitudinal cohort. A total of 32 patients with Alzheimer's disease, 49 subjects with mild cognitive impairment and 103 healthy controls underwent two Pittsburgh compound B-positron emission tomography scans 18 months apart. For each participant, a parametric map of Pittsburgh compound B-positron emission tomography rate of change was created [(follow-up scan - baseline scan)/ follow-up duration] and entered in a voxelwise three-way analysis of covariance, with clinical status (healthy controls, mild cognitive impairment or Alzheimer's disease), disease progression (clinical conversion from healthy controls to mild cognitive impairment or Alzheimer's disease, or from mild cognitive impairment to Alzheimer's disease) and Pittsburgh compound B status (positive versus negative) as independent factors. Only a significant effect of the Pittsburgh compound B status was found: both Pittsburgh compound B-positive and -negative subjects showed a significant increase in amyloid-β deposition, with this increase being significantly higher in Pittsburgh compound B-positive individuals. This finding suggests either that Pittsburgh compound B-negative individuals have slower rates of amyloid-β accumulation than positive, or that the proportion of individuals showing significant increase in amyloid-β deposition, termed 'Pittsburgh compound B accumulators', is higher within the Pittsburgh compound B-positive group than within the Pittsburgh compound B-negative group. The bimodal distribution of the individual rates of neocortical amyloid-β accumulation observed support the existence of 'Pittsburgh compound B non-accumulators' and 'Pittsburgh compound B accumulators' and different clustering analyses led to a consistent threshold to separate these two subgroups (0.014-0.022 standardized uptake value ratio<sub>pons</sub>
/year). The voxelwise three-way analysis of covariance was thus recomputed with the 'Pittsburgh compound B accumulators' only and the results were almost unchanged, with the Pittsburgh compound B-positive group showing higher accumulation than the Pittsburgh compound B-negative group. Finally, a significant negative correlation was found between Pittsburgh compound B rate of change and Pittsburgh compound B baseline burden, but only in the Pittsburgh compound B-positive group (r= -0.24; P=0.025). Higher rates of amyloid-β deposition are associated with higher amyloid-β burden suggesting that amyloid-β deposition does not reach a plateau when cognitive impairments manifest but is instead an ongoing process present even at the Alzheimer's disease stage. amyloid-β accumulation also seems to slow down at the latest stages of the process, i.e. in participants with the highest amyloid burden. Furthermore, this study identified the existence of Pittsburgh compound 'accumulators' and 'non-accumulators', notably within the Pittsburgh compound B-negative group, which may be a relevant concept for future studies.</div>
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<fC03 i1="07" i2="X" l="FRE"><s0>Tomoscintigraphie</s0>
<s5>11</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Emission tomography</s0>
<s5>11</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Tomocentelleografía</s0>
<s5>11</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Tomographie par émission de positons</s0>
<s5>12</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Positron emission tomography</s0>
<s5>12</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Tomografía emisión positrones</s0>
<s5>12</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Vieillissement</s0>
<s5>13</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Ageing</s0>
<s5>13</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Envejecimiento</s0>
<s5>13</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Homme</s0>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Human</s0>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Hombre</s0>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>38</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>39</s5>
</fC07>
<fN21><s1>212</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
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<server><NO>PASCAL 12-0279742 INIST</NO>
<ET>Regional dynamics of amyloid-β deposition in healthy elderly, mild cognitive impairment and Alzheimer's disease: a voxelwise PiB-PET longitudinal study</ET>
<AU>VILLAIN (Nicolas); CHETELAT (Gaël); GRASSIOT (Blandine); BOURGEAT (Pierrick); JONES (Gareth); ELLIS (Kathryn A.); AMES (David); MARTINS (Ralph N.); EUSTACHE (Francis); SALVADO (Olivier); MASTERS (Colin L.); ROWE (Christopher C.); VILLEMAGNE (Victor L.)</AU>
<AF>INSERM, U1077/Caen 14000/France (1 aut., 2 aut., 3 aut., 9 aut.); Université de Caen Basse-Normandie, UMR-S1077/Caen 14000/France (1 aut., 2 aut., 3 aut., 9 aut.); Ecole Pratique des Hautes Etudes, UMR-S1077/Caen 14000/France (1 aut., 2 aut., 3 aut., 9 aut.); CHU de Caen, U1077/Caen 14000/France (1 aut., 2 aut., 3 aut., 9 aut.); Department of Nuclear Medicine and Centre for PET, Austin Health, 145 Studley Road/Heidelberg, VIC 3084/Australie (2 aut., 5 aut., 12 aut., 13 aut.); CSIRO Preventative Health National Research Flagship ICTC, The Australian e-Health Research Centre, BioMedIA, Royal Brisbane and Women's Hospital/Herston, QLD 4006/Australie (4 aut., 10 aut.); Department of Psychiatry, University of Melbourne/Parkville, VIC 3052/Australie (6 aut., 7 aut.); Centre of Excellence for Alzheimer's Disease Research and Care, School of Exercise Biomedical and Health Sciences, Edith Cowan University/Joondalup, WA 6027/Australie (8 aut.); The Mental Health Research Institute, University of Melbourne/VIC 3000/Australie (6 aut., 11 aut., 13 aut.); Department of Medicine, Austin Health, University of Melbourne/VIC 3000/Australie (12 aut., 13 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Brain; ISSN 0006-8950; Royaume-Uni; Da. 2012; Vol. 135; No. p. 7; Pp. 2126-2139; Bibl. 1 p.1/4</SO>
<LA>Anglais</LA>
<EA>Amyloid-β deposition in Alzheimer's disease is thought to start while individuals are still cognitively unimpaired and it is hypothesized that after an early phase of fast accumulation, a plateau is reached by the time of cognitive decline. However, few longitudinal Pittsburgh compound B-positron emission tomography studies have tested this hypothesis, and with conflicting results. The purpose of this work is to further our understanding of the dynamics of amyloid-β deposition in a large longitudinal cohort. A total of 32 patients with Alzheimer's disease, 49 subjects with mild cognitive impairment and 103 healthy controls underwent two Pittsburgh compound B-positron emission tomography scans 18 months apart. For each participant, a parametric map of Pittsburgh compound B-positron emission tomography rate of change was created [(follow-up scan - baseline scan)/ follow-up duration] and entered in a voxelwise three-way analysis of covariance, with clinical status (healthy controls, mild cognitive impairment or Alzheimer's disease), disease progression (clinical conversion from healthy controls to mild cognitive impairment or Alzheimer's disease, or from mild cognitive impairment to Alzheimer's disease) and Pittsburgh compound B status (positive versus negative) as independent factors. Only a significant effect of the Pittsburgh compound B status was found: both Pittsburgh compound B-positive and -negative subjects showed a significant increase in amyloid-β deposition, with this increase being significantly higher in Pittsburgh compound B-positive individuals. This finding suggests either that Pittsburgh compound B-negative individuals have slower rates of amyloid-β accumulation than positive, or that the proportion of individuals showing significant increase in amyloid-β deposition, termed 'Pittsburgh compound B accumulators', is higher within the Pittsburgh compound B-positive group than within the Pittsburgh compound B-negative group. The bimodal distribution of the individual rates of neocortical amyloid-β accumulation observed support the existence of 'Pittsburgh compound B non-accumulators' and 'Pittsburgh compound B accumulators' and different clustering analyses led to a consistent threshold to separate these two subgroups (0.014-0.022 standardized uptake value ratio<sub>pons</sub>
/year). The voxelwise three-way analysis of covariance was thus recomputed with the 'Pittsburgh compound B accumulators' only and the results were almost unchanged, with the Pittsburgh compound B-positive group showing higher accumulation than the Pittsburgh compound B-negative group. Finally, a significant negative correlation was found between Pittsburgh compound B rate of change and Pittsburgh compound B baseline burden, but only in the Pittsburgh compound B-positive group (r= -0.24; P=0.025). Higher rates of amyloid-β deposition are associated with higher amyloid-β burden suggesting that amyloid-β deposition does not reach a plateau when cognitive impairments manifest but is instead an ongoing process present even at the Alzheimer's disease stage. amyloid-β accumulation also seems to slow down at the latest stages of the process, i.e. in participants with the highest amyloid burden. Furthermore, this study identified the existence of Pittsburgh compound 'accumulators' and 'non-accumulators', notably within the Pittsburgh compound B-negative group, which may be a relevant concept for future studies.</EA>
<CC>002B17; 002B17G</CC>
<FD>Déficit cognitif léger; Trouble cognitif; Démence d'Alzheimer; Pathologie du système nerveux; Amyloïde; Personne âgée; Tomoscintigraphie; Tomographie par émission de positons; Vieillissement</FD>
<FG>Homme; Pathologie de l'encéphale; Maladie dégénérative; Pathologie du système nerveux central</FG>
<ED>mild cognitive impairment; Cognitive disorder; Alzheimer disease; Nervous system diseases; Amyloid; Elderly; Emission tomography; Positron emission tomography; Ageing</ED>
<EG>Human; Cerebral disorder; Degenerative disease; Central nervous system disease</EG>
<SD>Disturbio cognitivo ligero; Trastorno cognitivo; Demencia Alzheimer; Sistema nervioso patología; Amiloide; Anciano; Tomocentelleografía; Tomografía emisión positrones; Envejecimiento</SD>
<LO>INIST-998.354000505272590120</LO>
<ID>12-0279742</ID>
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