AustralieFrV1, PascalFrancis, Curation, bibRecord, 003844

Relationship between Atrophy and β-Amyloid Deposition in Alzheimer Disease

Identifieur interne : 003844 ( PascalFrancis/Curation ); précédent : 003843; suivant : 003845

Relationship between Atrophy and β-Amyloid Deposition in Alzheimer Disease

Auteurs : Gaël Chetelat [Australie, France] ; Victor L. Villemagne [Australie] ; Pierrick Bourgeat [Australie] ; Kerryn E. Pike [Australie] ; Gareth Jones [Australie] ; David Ames [Australie] ; Kathryn A. Ellis [Australie] ; Cassandra Szoeke [Australie] ; Ralph N. Martins [Australie] ; Graeme J. O'Keefe [Australie] ; Olivier Salvado [Australie] ; Colin L. Masters [Australie] ; Christopher C. Rowe [Australie]

Source :

Annals of neurology [ 0364-5134 ] ; 2010.

RBID : Pascal:10-0201781

Descripteurs français

Pascal (Inist)
- Atrophie, Démence d'Alzheimer, Pathologie du système nerveux, Amyloïde.

English descriptors

KwdEn :
- Alzheimer disease, Amyloid, Atrophy, Nervous system diseases.

Abstract

Objective: Elucidating the role of aggregated β-amyloid in relation to gray matter atrophy is crucial to the understanding of the pathological mechanisms of Alzheimer disease and for the development of therapeutic trials. The present study aims to assess this relationship. Methods: Brain magnetic resonance imaging and [¹¹C]Pittsburgh compound B (PiB)-positron emission tomography scans were obtained from 94 healthy elderly subjects (49 with subjective cognitive impairment), 34 patients with mild cognitive impairment, and 35 patients with Alzheimer disease. The correlations between global and regional neocortical PiB retention and atrophy were analyzed in each clinical group. Results: Global and regional atrophy were strongly related to β-amyloid load in participants with subjective cognitive impairment but not in patients with mild cognitive impairment or Alzheimer disease. Global neocortical β-amyloid deposition correlated to atrophy in a large brain network including the hippocampus, medial frontal and parietal areas, and lateral temporoparietal cortex, whereas regional β-amyloid load was related to local atrophy in the areas of highest β-amyloid load only, that is, medial orbitofrontal and anterior and posterior cingulate/ precuneus areas. Interpretation: There is a strong relationship between β-amyloid deposition and atrophy very early in the disease process. As the disease progresses to mild cognitive impairment and Alzheimer disease clinical stages, pathological events other than, and probably downstream from, aggregated β-amyloid deposition might be responsible for the ongoing atrophic process. These findings suggest that antiamyloid therapy should be administered very early in the disease evolution to minimize synaptic and neuronal loss.

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A02	`01`			`@0 ANNED3`
A03		`1`		`@0 Ann. neurol.`
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A08	`01`	`1`	`ENG`	`@1 Relationship between Atrophy and β-Amyloid Deposition in Alzheimer Disease`
A11	`01`	`1`		`@1 CHETELAT (Gaël)`
A11	`02`	`1`		`@1 VILLEMAGNE (Victor L.)`
A11	`03`	`1`		`@1 BOURGEAT (Pierrick)`
A11	`04`	`1`		`@1 PIKE (Kerryn E.)`
A11	`05`	`1`		`@1 JONES (Gareth)`
A11	`06`	`1`		`@1 AMES (David)`
A11	`07`	`1`		`@1 ELLIS (Kathryn A.)`
A11	`08`	`1`		`@1 SZOEKE (Cassandra)`
A11	`09`	`1`		`@1 MARTINS (Ralph N.)`
A11	`10`	`1`		`@1 O'KEEFE (Graeme J.)`
A11	`11`	`1`		`@1 SALVADO (Olivier)`
A11	`12`	`1`		`@1 MASTERS (Colin L.)`
A11	`13`	`1`		`@1 ROWE (Christopher C.)`
A14	`01`			`@1 Department of Nuclear Medicine and Center for PET, Austin Health @2 Heidelberg @3 AUS @Z 1 aut. @Z 2 aut. @Z 4 aut. @Z 5 aut. @Z 10 aut. @Z 13 aut.`
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A14	`06`			`@1 National Ageing Research Institute @2 Melbourne @3 AUS @Z 6 aut.`
A14	`07`			`@1 Academic Unit for Psychiatry of Old Age, Department of Psychiatry, University of Melbourne, St. Vincent's Aged Psychiatry Service, St George's Hospital @2 Melbourne @3 AUS @Z 7 aut.`
A14	`08`			`@1 Centre of Excellence for Alzheimer's Disease Research & Care, School of Exercise, Biomedical, and Health Sciences, Edith Cowan University @2 Joondalup @3 AUS @Z 9 aut.`
A17	`01`	`1`		`@1 Australian Imaging Biomarkers and Lifestyle Research Group @3 AUS`
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A21				`@1 2010`
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A64	`01`	`1`		`@0 Annals of neurology`
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C01	`01`		`ENG`	@0 Objective: Elucidating the role of aggregated β-amyloid in relation to gray matter atrophy is crucial to the understanding of the pathological mechanisms of Alzheimer disease and for the development of therapeutic trials. The present study aims to assess this relationship. Methods: Brain magnetic resonance imaging and [¹¹C]Pittsburgh compound B (PiB)-positron emission tomography scans were obtained from 94 healthy elderly subjects (49 with subjective cognitive impairment), 34 patients with mild cognitive impairment, and 35 patients with Alzheimer disease. The correlations between global and regional neocortical PiB retention and atrophy were analyzed in each clinical group. Results: Global and regional atrophy were strongly related to β-amyloid load in participants with subjective cognitive impairment but not in patients with mild cognitive impairment or Alzheimer disease. Global neocortical β-amyloid deposition correlated to atrophy in a large brain network including the hippocampus, medial frontal and parietal areas, and lateral temporoparietal cortex, whereas regional β-amyloid load was related to local atrophy in the areas of highest β-amyloid load only, that is, medial orbitofrontal and anterior and posterior cingulate/ precuneus areas. Interpretation: There is a strong relationship between β-amyloid deposition and atrophy very early in the disease process. As the disease progresses to mild cognitive impairment and Alzheimer disease clinical stages, pathological events other than, and probably downstream from, aggregated β-amyloid deposition might be responsible for the ongoing atrophic process. These findings suggest that antiamyloid therapy should be administered very early in the disease evolution to minimize synaptic and neuronal loss.
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C03	`01`	`X`	`FRE`	`@0 Atrophie @5 01`
C03	`01`	`X`	`ENG`	`@0 Atrophy @5 01`
C03	`01`	`X`	`SPA`	`@0 Atrofia @5 01`
C03	`02`	`X`	`FRE`	`@0 Démence d'Alzheimer @5 02`
C03	`02`	`X`	`ENG`	`@0 Alzheimer disease @5 02`
C03	`02`	`X`	`SPA`	`@0 Demencia Alzheimer @5 02`
C03	`03`	`X`	`FRE`	`@0 Pathologie du système nerveux @5 03`
C03	`03`	`X`	`ENG`	`@0 Nervous system diseases @5 03`
C03	`03`	`X`	`SPA`	`@0 Sistema nervioso patología @5 03`
C03	`04`	`X`	`FRE`	`@0 Amyloïde @5 09`
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C03	`04`	`X`	`SPA`	`@0 Amiloide @5 09`
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`
C07	`03`	`X`	`ENG`	`@0 Central nervous system disease @5 39`
C07	`03`	`X`	`SPA`	`@0 Sistema nervosio central patología @5 39`
N21				`@1 130`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

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Le document en format XML

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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>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Relationship between Atrophy and β-Amyloid Deposition in Alzheimer Disease</title>
<author><name sortKey="Chetelat, Gael" sort="Chetelat, Gael" uniqKey="Chetelat G" first="Gaël" last="Chetelat">Gaël Chetelat</name>
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</author>
<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="Bourgeat, Pierrick" sort="Bourgeat, Pierrick" uniqKey="Bourgeat P" first="Pierrick" last="Bourgeat">Pierrick Bourgeat</name>
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</author>
<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 and Center for PET, Austin Health</s1>
<s2>Heidelberg</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
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<sZ>13 aut.</sZ>
</inist:fA14>
<country>Australie</country>
</affiliation>
<affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Mental Health Research Institute, University of Melbourne</s1>
<s2>Melbourne</s2>
<s3>AUS</s3>
<sZ>2 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>12 aut.</sZ>
</inist:fA14>
<country>Australie</country>
</affiliation>
</author>
<author><name sortKey="Jones, Gareth" sort="Jones, Gareth" uniqKey="Jones G" first="Gareth" last="Jones">Gareth Jones</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Nuclear Medicine and Center for PET, Austin Health</s1>
<s2>Heidelberg</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>4 aut.</sZ>
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<sZ>10 aut.</sZ>
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</inist:fA14>
<country>Australie</country>
</affiliation>
</author>
<author><name sortKey="Ames, David" sort="Ames, David" uniqKey="Ames D" first="David" last="Ames">David Ames</name>
<affiliation wicri:level="1"><inist:fA14 i1="06"><s1>National Ageing Research Institute</s1>
<s2>Melbourne</s2>
<s3>AUS</s3>
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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="07"><s1>Academic Unit for Psychiatry of Old Age, Department of Psychiatry, University of Melbourne, St. Vincent's Aged Psychiatry Service, St George's Hospital</s1>
<s2>Melbourne</s2>
<s3>AUS</s3>
<sZ>7 aut.</sZ>
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<country>Australie</country>
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<author><name sortKey="Szoeke, Cassandra" sort="Szoeke, Cassandra" uniqKey="Szoeke C" first="Cassandra" last="Szoeke">Cassandra Szoeke</name>
<affiliation wicri:level="1"><inist:fA14 i1="05"><s1>CSIRO Preventative Health National Research Flagship ICTC, Australian e-Health Research Centre, BioMedIA, Royal Brisbane and Women's Hospital</s1>
<s2>Herston</s2>
<s3>AUS</s3>
<sZ>3 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
<country>Australie</country>
</affiliation>
</author>
<author><name sortKey="Martins, Ralph N" sort="Martins, Ralph N" uniqKey="Martins R" first="Ralph N." last="Martins">Ralph N. Martins</name>
<affiliation wicri:level="1"><inist:fA14 i1="08"><s1>Centre of Excellence for Alzheimer's Disease Research & Care, School of Exercise, Biomedical, and Health Sciences, Edith Cowan University</s1>
<s2>Joondalup</s2>
<s3>AUS</s3>
<sZ>9 aut.</sZ>
</inist:fA14>
<country>Australie</country>
</affiliation>
</author>
<author><name sortKey="O Keefe, Graeme J" sort="O Keefe, Graeme J" uniqKey="O Keefe G" first="Graeme J." last="O'Keefe">Graeme J. O'Keefe</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Nuclear Medicine and Center for PET, Austin Health</s1>
<s2>Heidelberg</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>13 aut.</sZ>
</inist:fA14>
<country>Australie</country>
</affiliation>
</author>
<author><name sortKey="Salvado, Olivier" sort="Salvado, Olivier" uniqKey="Salvado O" first="Olivier" last="Salvado">Olivier Salvado</name>
<affiliation wicri:level="1"><inist:fA14 i1="05"><s1>CSIRO Preventative Health National Research Flagship ICTC, Australian e-Health Research Centre, BioMedIA, Royal Brisbane and Women's Hospital</s1>
<s2>Herston</s2>
<s3>AUS</s3>
<sZ>3 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
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<country>Australie</country>
</affiliation>
</author>
<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="03"><s1>Mental Health Research Institute, University of Melbourne</s1>
<s2>Melbourne</s2>
<s3>AUS</s3>
<sZ>2 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>12 aut.</sZ>
</inist:fA14>
<country>Australie</country>
</affiliation>
</author>
<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 and Center for PET, Austin Health</s1>
<s2>Heidelberg</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>13 aut.</sZ>
</inist:fA14>
<country>Australie</country>
</affiliation>
<affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Department of Medicine, Austin Health, University of Melbourne</s1>
<s2>Heidelberg</s2>
<s3>AUS</s3>
<sZ>2 aut.</sZ>
<sZ>13 aut.</sZ>
</inist:fA14>
<country>Australie</country>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">Annals of neurology</title>
<title level="j" type="abbreviated">Ann. neurol.</title>
<idno type="ISSN">0364-5134</idno>
<imprint><date when="2010">2010</date>
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<seriesStmt><title level="j" type="main">Annals of neurology</title>
<title level="j" type="abbreviated">Ann. neurol.</title>
<idno type="ISSN">0364-5134</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alzheimer disease</term>
<term>Amyloid</term>
<term>Atrophy</term>
<term>Nervous system diseases</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Atrophie</term>
<term>Démence d'Alzheimer</term>
<term>Pathologie du   système nerveux</term>
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<front><div type="abstract" xml:lang="en">Objective: Elucidating the role of aggregated β-amyloid in relation to gray matter atrophy is crucial to the understanding of the pathological mechanisms of Alzheimer disease and for the development of therapeutic trials. The present study aims to assess this relationship. Methods: Brain magnetic resonance imaging and [<sup>11</sup>
C]Pittsburgh compound B (PiB)-positron emission tomography scans were obtained from 94 healthy elderly subjects (49 with subjective cognitive impairment), 34 patients with mild cognitive impairment, and 35 patients with Alzheimer disease. The correlations between global and regional neocortical PiB retention and atrophy were analyzed in each clinical group. Results: Global and regional atrophy were strongly related to β-amyloid load in participants with subjective cognitive impairment but not in patients with mild cognitive impairment or Alzheimer disease. Global neocortical β-amyloid deposition correlated to atrophy in a large brain network including the hippocampus, medial frontal and parietal areas, and lateral temporoparietal cortex, whereas regional β-amyloid load was related to local atrophy in the areas of highest β-amyloid load only, that is, medial orbitofrontal and anterior and posterior cingulate/ precuneus areas. Interpretation: There is a strong relationship between β-amyloid deposition and atrophy very early in the disease process. As the disease progresses to mild cognitive impairment and Alzheimer disease clinical stages, pathological events other than, and probably downstream from, aggregated β-amyloid deposition might be responsible for the ongoing atrophic process. These findings suggest that antiamyloid therapy should be administered very early in the disease evolution to minimize synaptic and neuronal loss.</div>
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<fA08 i1="01" i2="1" l="ENG"><s1>Relationship between Atrophy and β-Amyloid Deposition in Alzheimer Disease</s1>
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<fA14 i1="01"><s1>Department of Nuclear Medicine and Center for PET, Austin Health</s1>
<s2>Heidelberg</s2>
<s3>AUS</s3>
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<fA14 i1="02"><s1>Inserm-EPHE-University of Caen/Basse-Normandie, Unit U923, GIP Cyceron, CHU Côte de Nacre</s1>
<s2>Caen</s2>
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<fA14 i1="03"><s1>Mental Health Research Institute, University of Melbourne</s1>
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<sZ>12 aut.</sZ>
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<fA14 i1="04"><s1>Department of Medicine, Austin Health, University of Melbourne</s1>
<s2>Heidelberg</s2>
<s3>AUS</s3>
<sZ>2 aut.</sZ>
<sZ>13 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>CSIRO Preventative Health National Research Flagship ICTC, Australian e-Health Research Centre, BioMedIA, Royal Brisbane and Women's Hospital</s1>
<s2>Herston</s2>
<s3>AUS</s3>
<sZ>3 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>National Ageing Research Institute</s1>
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<s3>AUS</s3>
<sZ>7 aut.</sZ>
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<fA14 i1="08"><s1>Centre of Excellence for Alzheimer's Disease Research & Care, School of Exercise, Biomedical, and Health Sciences, Edith Cowan University</s1>
<s2>Joondalup</s2>
<s3>AUS</s3>
<sZ>9 aut.</sZ>
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C]Pittsburgh compound B (PiB)-positron emission tomography scans were obtained from 94 healthy elderly subjects (49 with subjective cognitive impairment), 34 patients with mild cognitive impairment, and 35 patients with Alzheimer disease. The correlations between global and regional neocortical PiB retention and atrophy were analyzed in each clinical group. Results: Global and regional atrophy were strongly related to β-amyloid load in participants with subjective cognitive impairment but not in patients with mild cognitive impairment or Alzheimer disease. Global neocortical β-amyloid deposition correlated to atrophy in a large brain network including the hippocampus, medial frontal and parietal areas, and lateral temporoparietal cortex, whereas regional β-amyloid load was related to local atrophy in the areas of highest β-amyloid load only, that is, medial orbitofrontal and anterior and posterior cingulate/ precuneus areas. Interpretation: There is a strong relationship between β-amyloid deposition and atrophy very early in the disease process. As the disease progresses to mild cognitive impairment and Alzheimer disease clinical stages, pathological events other than, and probably downstream from, aggregated β-amyloid deposition might be responsible for the ongoing atrophic process. These findings suggest that antiamyloid therapy should be administered very early in the disease evolution to minimize synaptic and neuronal loss.</s0>
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Relationship between Atrophy and β-Amyloid Deposition in Alzheimer Disease

Relationship between Atrophy and β-Amyloid Deposition in Alzheimer Disease

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