Larger temporal volume in elderly with high versus low beta-amyloid deposition
Identifieur interne : 002249 ( PascalFrancis/Corpus ); précédent : 002248; suivant : 002250Larger temporal volume in elderly with high versus low beta-amyloid deposition
Auteurs : Gaël Chetelat ; Victor L. Villemagne ; Kerryn E. Pike ; Jean-Claude Baron ; Pierrick Bourgeat ; Gareth Jones ; Noel G. Faux ; Kathryn A. Ellis ; Olivier Salvado ; Cassandra Szoeke ; Ralph N. Martins ; David Ames ; Colin L. Masters ; Christopher C. RoweSource :
- Brain [ 0006-8950 ] ; 2010.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
β-Amyloid deposition is one of the main hallmarks of Alzheimer's disease thought to eventually cause neuronal death. Post-mortem and neuroimaging studies have consistently reported cases with documented normal cognition despite high β-amylold burden. It is of great interest to understand what differentiates these particular subjects from those without β-amyloid deposition or with both β-amyloid deposition and cognitive deficits, i.e. what allows these subjects to resist the damage of the pathological lesions. [11C]Pittsburgh compound B positron emission tomography and magnetic resonance brain scans were obtained in 149 participants including healthy controls and patients with subjective cognitive impairment, mild cognitive impairment and Alzheimer's disease. Magnetic resonance data were compared between high versus low-[11C]Pittsburgh compound B cases, and between high-[11C]Pittsburgh compound B cases with versus those without cognitive deficits. Larger temporal (including hippocampal) grey matter volume, associated with better episodic memory performance, was found in high- versus low-[11C]Pittsburgh compound B healthy controls. The same finding was obtained using different [11C]Pittsburgh compound B thresholds, correcting [11C]Pittsburgh compound B data for partial averaging, using age, education, Mini-Mental State Examination, apolipoprotein E4 and sex-matched subsamples, and using manual hippocampal delineation instead of voxel-based analysis. By contrast, in participants with subjective cognitive impairment, significant grey matter atrophy was found in high-[11C]Pittsburgh compound B cases compared to low-[11C]Pittsburgh compound B cases, as well as in high-[11C]Pittsburgh compound B cases with subjective cognitive impairment, mild cognitive impairment and Alzheimer's disease compared to high-[11C]Pittsburgh compound B healthy controls. Larger grey matter volume in high-[11C]Pittsburgh compound B healthy controls may reflect either a tissue reactive response to β-amyloid or a combination of higher 'brain reserve' and under-representation of subjects with standard/low temporal volume in the high-[11C]Pittsburgh compound B healthy controls. Our complementary analyses tend to support the latter hypotheses. Overall, our findings suggest that the deleterious effects of β-amyloid on cognition may be delayed in those subjects with larger brain (temporal) volume.
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Format Inist (serveur)
| NO : | PASCAL 10-0515981 INIST |
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| ET : | Larger temporal volume in elderly with high versus low beta-amyloid deposition |
| AU : | CHETELAT (Gaël); VILLEMAGNE (Victor L.); PIKE (Kerryn E.); BARON (Jean-Claude); BOURGEAT (Pierrick); JONES (Gareth); FAUX (Noel G.); ELLIS (Kathryn A.); SALVADO (Olivier); SZOEKE (Cassandra); MARTINS (Ralph N.); AMES (David); MASTERS (Colin L.); ROWE (Christopher C.) |
| AF : | Department of Nuclear Medicine and Centre for PET, Austin Health/Heidelberg, VIC 3084/Australie (1 aut., 2 aut., 3 aut., 6 aut., 14 aut.); Inserm-EPHE-Université de Caen/Basse-Normandie, Unité U923, GIP Cyceron, CHU Côte de Nacre/14074 Caen/France (1 aut.); The Mental Health Research Institute, The University of Melbourne/Melbourne, VIC 3052/Australie (2 aut., 3 aut., 7 aut., 13 aut.); Department of Medicine, Austin Health, The University of Melbourne/Melbourne, VIC 3052/Australie (2 aut., 14 aut.); Department of Clinical Neurosciences, Neurology Unit, University of Cambridge/Cambridge CB2 2QQ/Royaume-Uni (4 aut.); CSIRO Preventative Health National Research Flagship ICTC, The Australian e-Health Research Centre, BioMedlA, Royal Brisbane and Women's Hospital/Herston, QLD 4006/Australie (5 aut., 9 aut.); Academic Unit for Psychiatry of Old Age, Department of Psychiatry, The University of Melbourne, St. Vincent's Aged Psychiatry Service, St George's Hospital/Melbourne VIC 3101/Australie (8 aut.); CSIRO Neurodegenerative Disease, Mental Disorders & Brain Health, Preventative Health Flagship, CSIRO Molecular and Health Technologies, Parkville/Melbourne, VIC 3052/Australie (10 aut.); Centre of Excellence for Alzheimer's Disease Research & Care, School of Exercise Biomedical and Health Sciences, Edith Cowan University/Joondalup, WA 6027/Australie (11 aut.); National Ageing Research Institute/Melbourne, VIC 3052/Australie (12 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Brain; ISSN 0006-8950; Royaume-Uni; Da. 2010; Vol. 133; No. p. 11; Pp. 3349-3358; Bibl. 3/4 p. |
| LA : | Anglais |
| EA : | β-Amyloid deposition is one of the main hallmarks of Alzheimer's disease thought to eventually cause neuronal death. Post-mortem and neuroimaging studies have consistently reported cases with documented normal cognition despite high β-amylold burden. It is of great interest to understand what differentiates these particular subjects from those without β-amyloid deposition or with both β-amyloid deposition and cognitive deficits, i.e. what allows these subjects to resist the damage of the pathological lesions. [11C]Pittsburgh compound B positron emission tomography and magnetic resonance brain scans were obtained in 149 participants including healthy controls and patients with subjective cognitive impairment, mild cognitive impairment and Alzheimer's disease. Magnetic resonance data were compared between high versus low-[11C]Pittsburgh compound B cases, and between high-[11C]Pittsburgh compound B cases with versus those without cognitive deficits. Larger temporal (including hippocampal) grey matter volume, associated with better episodic memory performance, was found in high- versus low-[11C]Pittsburgh compound B healthy controls. The same finding was obtained using different [11C]Pittsburgh compound B thresholds, correcting [11C]Pittsburgh compound B data for partial averaging, using age, education, Mini-Mental State Examination, apolipoprotein E4 and sex-matched subsamples, and using manual hippocampal delineation instead of voxel-based analysis. By contrast, in participants with subjective cognitive impairment, significant grey matter atrophy was found in high-[11C]Pittsburgh compound B cases compared to low-[11C]Pittsburgh compound B cases, as well as in high-[11C]Pittsbur gh compound B cases with subjective cognitive impairment, mild cognitive impairment and Alzheimer's disease compared to high-[11C]Pittsburgh compound B healthy controls. Larger grey matter volume in high-[11C]Pittsburgh compound B healthy controls may reflect either a tissue reactive response to β-amyloid or a combination of higher 'brain reserve' and under-representation of subjects with standard/low temporal volume in the high-[11C]Pittsburgh compound B healthy controls. Our complementary analyses tend to support the latter hypotheses. Overall, our findings suggest that the deleterious effects of β-amyloid on cognition may be delayed in those subjects with larger brain (temporal) volume. |
| CC : | 002B17; 002B17A03 |
| FD : | Démence d'Alzheimer; Atrophie; Pathologie du système nerveux; Personne âgée; Etude comparative; Amyloïde; Tomoscintigraphie; Tomographie par émission de positons |
| FG : | Homme; Pathologie de l'encéphale; Maladie dégénérative; Pathologie du système nerveux central |
| ED : | Alzheimer disease; Atrophy; Nervous system diseases; Elderly; Comparative study; Amyloid; Emission tomography; Positron emission tomography |
| EG : | Human; Cerebral disorder; Degenerative disease; Central nervous system disease |
| SD : | Demencia Alzheimer; Atrofia; Sistema nervioso patología; Anciano; Estudio comparativo; Amiloide; Tomocentelleografía; Tomografía emisión positrones |
| LO : | INIST-998.354000193438630170 |
| ID : | 10-0515981 |
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Martins</name><affiliation><inist:fA14 i1="09"><s1>Centre of Excellence for Alzheimer's Disease Research & Care, School of Exercise Biomedical and Health Sciences, Edith Cowan University</s1><s2>Joondalup, WA 6027</s2><s3>AUS</s3><sZ>11 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Ames, David" sort="Ames, David" uniqKey="Ames D" first="David" last="Ames">David Ames</name><affiliation><inist:fA14 i1="10"><s1>National Ageing Research Institute</s1><s2>Melbourne, VIC 3052</s2><s3>AUS</s3><sZ>12 aut.</sZ></inist:fA14></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><inist:fA14 i1="03"><s1>The Mental Health Research Institute, The University of Melbourne</s1><s2>Melbourne, VIC 3052</s2><s3>AUS</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>7 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></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><inist:fA14 i1="01"><s1>Department of Nuclear Medicine and Centre for PET, Austin Health</s1><s2>Heidelberg, VIC 3084</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Department of Medicine, Austin Health, The University of Melbourne</s1><s2>Melbourne, VIC 3052</s2><s3>AUS</s3><sZ>2 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">10-0515981</idno><date when="2010">2010</date><idno type="stanalyst">PASCAL 10-0515981 INIST</idno><idno type="RBID">Pascal:10-0515981</idno><idno type="wicri:Area/PascalFrancis/Corpus">002249</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Larger temporal volume in elderly with high versus low beta-amyloid deposition</title><author><name sortKey="Chetelat, Gael" sort="Chetelat, Gael" uniqKey="Chetelat G" first="Gaël" last="Chetelat">Gaël Chetelat</name><affiliation><inist:fA14 i1="01"><s1>Department of Nuclear Medicine and Centre for PET, Austin Health</s1><s2>Heidelberg, VIC 3084</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Inserm-EPHE-Université de Caen/Basse-Normandie, Unité U923, GIP Cyceron, CHU Côte de Nacre</s1><s2>14074 Caen</s2><s3>FRA</s3><sZ>1 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Villemagne, Victor L" sort="Villemagne, Victor L" uniqKey="Villemagne V" first="Victor L." last="Villemagne">Victor L. Villemagne</name><affiliation><inist:fA14 i1="01"><s1>Department of Nuclear Medicine and Centre for PET, Austin Health</s1><s2>Heidelberg, VIC 3084</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>The Mental Health Research Institute, The University of Melbourne</s1><s2>Melbourne, VIC 3052</s2><s3>AUS</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>7 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Department of Medicine, Austin Health, The University of Melbourne</s1><s2>Melbourne, VIC 3052</s2><s3>AUS</s3><sZ>2 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Pike, Kerryn E" sort="Pike, Kerryn E" uniqKey="Pike K" first="Kerryn E." last="Pike">Kerryn E. Pike</name><affiliation><inist:fA14 i1="01"><s1>Department of Nuclear Medicine and Centre for PET, Austin Health</s1><s2>Heidelberg, VIC 3084</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>The Mental Health Research Institute, The University of Melbourne</s1><s2>Melbourne, VIC 3052</s2><s3>AUS</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>7 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Baron, Jean Claude" sort="Baron, Jean Claude" uniqKey="Baron J" first="Jean-Claude" last="Baron">Jean-Claude Baron</name><affiliation><inist:fA14 i1="05"><s1>Department of Clinical Neurosciences, Neurology Unit, University of Cambridge</s1><s2>Cambridge CB2 2QQ</s2><s3>GBR</s3><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Bourgeat, Pierrick" sort="Bourgeat, Pierrick" uniqKey="Bourgeat P" first="Pierrick" last="Bourgeat">Pierrick Bourgeat</name><affiliation><inist:fA14 i1="06"><s1>CSIRO Preventative Health National Research Flagship ICTC, The Australian e-Health Research Centre, BioMedlA, Royal Brisbane and Women's Hospital</s1><s2>Herston, QLD 4006</s2><s3>AUS</s3><sZ>5 aut.</sZ><sZ>9 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Jones, Gareth" sort="Jones, Gareth" uniqKey="Jones G" first="Gareth" last="Jones">Gareth Jones</name><affiliation><inist:fA14 i1="01"><s1>Department of Nuclear Medicine and Centre for PET, Austin Health</s1><s2>Heidelberg, VIC 3084</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Faux, Noel G" sort="Faux, Noel G" uniqKey="Faux N" first="Noel G." last="Faux">Noel G. Faux</name><affiliation><inist:fA14 i1="03"><s1>The Mental Health Research Institute, The University of Melbourne</s1><s2>Melbourne, VIC 3052</s2><s3>AUS</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>7 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Ellis, Kathryn A" sort="Ellis, Kathryn A" uniqKey="Ellis K" first="Kathryn A." last="Ellis">Kathryn A. Ellis</name><affiliation><inist:fA14 i1="07"><s1>Academic Unit for Psychiatry of Old Age, Department of Psychiatry, The University of Melbourne, St. Vincent's Aged Psychiatry Service, St George's Hospital</s1><s2>Melbourne VIC 3101</s2><s3>AUS</s3><sZ>8 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Salvado, Olivier" sort="Salvado, Olivier" uniqKey="Salvado O" first="Olivier" last="Salvado">Olivier Salvado</name><affiliation><inist:fA14 i1="06"><s1>CSIRO Preventative Health National Research Flagship ICTC, The Australian e-Health Research Centre, BioMedlA, Royal Brisbane and Women's Hospital</s1><s2>Herston, QLD 4006</s2><s3>AUS</s3><sZ>5 aut.</sZ><sZ>9 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Szoeke, Cassandra" sort="Szoeke, Cassandra" uniqKey="Szoeke C" first="Cassandra" last="Szoeke">Cassandra Szoeke</name><affiliation><inist:fA14 i1="08"><s1>CSIRO Neurodegenerative Disease, Mental Disorders & Brain Health, Preventative Health Flagship, CSIRO Molecular and Health Technologies, Parkville</s1><s2>Melbourne, VIC 3052</s2><s3>AUS</s3><sZ>10 aut.</sZ></inist:fA14></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><inist:fA14 i1="09"><s1>Centre of Excellence for Alzheimer's Disease Research & Care, School of Exercise Biomedical and Health Sciences, Edith Cowan University</s1><s2>Joondalup, WA 6027</s2><s3>AUS</s3><sZ>11 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Ames, David" sort="Ames, David" uniqKey="Ames D" first="David" last="Ames">David Ames</name><affiliation><inist:fA14 i1="10"><s1>National Ageing Research Institute</s1><s2>Melbourne, VIC 3052</s2><s3>AUS</s3><sZ>12 aut.</sZ></inist:fA14></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><inist:fA14 i1="03"><s1>The Mental Health Research Institute, The University of Melbourne</s1><s2>Melbourne, VIC 3052</s2><s3>AUS</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>7 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></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><inist:fA14 i1="01"><s1>Department of Nuclear Medicine and Centre for PET, Austin Health</s1><s2>Heidelberg, VIC 3084</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Department of Medicine, Austin Health, The University of Melbourne</s1><s2>Melbourne, VIC 3052</s2><s3>AUS</s3><sZ>2 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">Brain</title><title level="j" type="abbreviated">Brain</title><idno type="ISSN">0006-8950</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Brain</title><title level="j" type="abbreviated">Brain</title><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alzheimer disease</term><term>Amyloid</term><term>Atrophy</term><term>Comparative study</term><term>Elderly</term><term>Emission tomography</term><term>Nervous system diseases</term><term>Positron emission tomography</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Démence d'Alzheimer</term><term>Atrophie</term><term>Pathologie du système nerveux</term><term>Personne âgée</term><term>Etude comparative</term><term>Amyloïde</term><term>Tomoscintigraphie</term><term>Tomographie par émission de positons</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">β-Amyloid deposition is one of the main hallmarks of Alzheimer's disease thought to eventually cause neuronal death. Post-mortem and neuroimaging studies have consistently reported cases with documented normal cognition despite high β-amylold burden. It is of great interest to understand what differentiates these particular subjects from those without β-amyloid deposition or with both β-amyloid deposition and cognitive deficits, i.e. what allows these subjects to resist the damage of the pathological lesions. [<sup>11</sup>C]Pittsburgh compound B positron emission tomography and magnetic resonance brain scans were obtained in 149 participants including healthy controls and patients with subjective cognitive impairment, mild cognitive impairment and Alzheimer's disease. Magnetic resonance data were compared between high versus low-[11C]Pittsburgh compound B cases, and between high-[<sup>11</sup>C]Pittsburgh compound B cases with versus those without cognitive deficits. Larger temporal (including hippocampal) grey matter volume, associated with better episodic memory performance, was found in high- versus low-[<sup>11</sup>C]Pittsburgh compound B healthy controls. The same finding was obtained using different [<sup>11</sup>C]Pittsburgh compound B thresholds, correcting [<sup>11</sup>C]Pittsburgh compound B data for partial averaging, using age, education, Mini-Mental State Examination, apolipoprotein E4 and sex-matched subsamples, and using manual hippocampal delineation instead of voxel-based analysis. By contrast, in participants with subjective cognitive impairment, significant grey matter atrophy was found in high-[<sup>11</sup>C]Pittsburgh compound B cases compared to low-[<sup>11</sup>C]Pittsburgh compound B cases, as well as in high-[<sup>11</sup>C]Pittsburgh compound B cases with subjective cognitive impairment, mild cognitive impairment and Alzheimer's disease compared to high-[<sup>11</sup>C]Pittsburgh compound B healthy controls. Larger grey matter volume in high-[<sup>11</sup>C]Pittsburgh compound B healthy controls may reflect either a tissue reactive response to β-amyloid or a combination of higher 'brain reserve' and under-representation of subjects with standard/low temporal volume in the high-[<sup>11</sup>C]Pittsburgh compound B healthy controls. Our complementary analyses tend to support the latter hypotheses. Overall, our findings suggest that the deleterious effects of β-amyloid on cognition may be delayed in those subjects with larger brain (temporal) volume.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0006-8950</s0></fA01><fA03 i2="1"><s0>Brain</s0></fA03><fA05><s2>133</s2></fA05><fA06><s3>p. 11</s3></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Larger temporal volume in elderly with high versus low beta-amyloid deposition</s1></fA08><fA11 i1="01" i2="1"><s1>CHETELAT (Gaël)</s1></fA11><fA11 i1="02" i2="1"><s1>VILLEMAGNE (Victor L.)</s1></fA11><fA11 i1="03" i2="1"><s1>PIKE (Kerryn E.)</s1></fA11><fA11 i1="04" i2="1"><s1>BARON (Jean-Claude)</s1></fA11><fA11 i1="05" i2="1"><s1>BOURGEAT (Pierrick)</s1></fA11><fA11 i1="06" i2="1"><s1>JONES (Gareth)</s1></fA11><fA11 i1="07" i2="1"><s1>FAUX (Noel G.)</s1></fA11><fA11 i1="08" i2="1"><s1>ELLIS (Kathryn A.)</s1></fA11><fA11 i1="09" i2="1"><s1>SALVADO (Olivier)</s1></fA11><fA11 i1="10" i2="1"><s1>SZOEKE (Cassandra)</s1></fA11><fA11 i1="11" i2="1"><s1>MARTINS (Ralph N.)</s1></fA11><fA11 i1="12" i2="1"><s1>AMES (David)</s1></fA11><fA11 i1="13" i2="1"><s1>MASTERS (Colin L.)</s1></fA11><fA11 i1="14" i2="1"><s1>ROWE (Christopher C.)</s1></fA11><fA14 i1="01"><s1>Department of Nuclear Medicine and Centre for PET, Austin Health</s1><s2>Heidelberg, VIC 3084</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>14 aut.</sZ></fA14><fA14 i1="02"><s1>Inserm-EPHE-Université de Caen/Basse-Normandie, Unité U923, GIP Cyceron, CHU Côte de Nacre</s1><s2>14074 Caen</s2><s3>FRA</s3><sZ>1 aut.</sZ></fA14><fA14 i1="03"><s1>The Mental Health Research Institute, The University of Melbourne</s1><s2>Melbourne, VIC 3052</s2><s3>AUS</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>7 aut.</sZ><sZ>13 aut.</sZ></fA14><fA14 i1="04"><s1>Department of Medicine, Austin Health, The University of Melbourne</s1><s2>Melbourne, VIC 3052</s2><s3>AUS</s3><sZ>2 aut.</sZ><sZ>14 aut.</sZ></fA14><fA14 i1="05"><s1>Department of Clinical Neurosciences, Neurology Unit, University of Cambridge</s1><s2>Cambridge CB2 2QQ</s2><s3>GBR</s3><sZ>4 aut.</sZ></fA14><fA14 i1="06"><s1>CSIRO Preventative Health National Research Flagship ICTC, The Australian e-Health Research Centre, BioMedlA, Royal Brisbane and Women's Hospital</s1><s2>Herston, QLD 4006</s2><s3>AUS</s3><sZ>5 aut.</sZ><sZ>9 aut.</sZ></fA14><fA14 i1="07"><s1>Academic Unit for Psychiatry of Old Age, Department of Psychiatry, The University of Melbourne, St. Vincent's Aged Psychiatry Service, St George's Hospital</s1><s2>Melbourne VIC 3101</s2><s3>AUS</s3><sZ>8 aut.</sZ></fA14><fA14 i1="08"><s1>CSIRO Neurodegenerative Disease, Mental Disorders & Brain Health, Preventative Health Flagship, CSIRO Molecular and Health Technologies, Parkville</s1><s2>Melbourne, VIC 3052</s2><s3>AUS</s3><sZ>10 aut.</sZ></fA14><fA14 i1="09"><s1>Centre of Excellence for Alzheimer's Disease Research & Care, School of Exercise Biomedical and Health Sciences, Edith Cowan University</s1><s2>Joondalup, WA 6027</s2><s3>AUS</s3><sZ>11 aut.</sZ></fA14><fA14 i1="10"><s1>National Ageing Research Institute</s1><s2>Melbourne, VIC 3052</s2><s3>AUS</s3><sZ>12 aut.</sZ></fA14><fA17 i1="01" i2="1"><s1>Australian Imaging Biomarkers and Lifestyle Study of Ageing (AIBL) Research Group</s1><s3>AUS</s3></fA17><fA20><s1>3349-3358</s1></fA20><fA21><s1>2010</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>998</s2><s5>354000193438630170</s5></fA43><fA44><s0>0000</s0><s1>© 2010 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>3/4 p.</s0></fA45><fA47 i1="01" i2="1"><s0>10-0515981</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Brain</s0></fA64><fA66 i1="01"><s0>GBR</s0></fA66><fC01 i1="01" l="ENG"><s0>β-Amyloid deposition is one of the main hallmarks of Alzheimer's disease thought to eventually cause neuronal death. Post-mortem and neuroimaging studies have consistently reported cases with documented normal cognition despite high β-amylold burden. It is of great interest to understand what differentiates these particular subjects from those without β-amyloid deposition or with both β-amyloid deposition and cognitive deficits, i.e. what allows these subjects to resist the damage of the pathological lesions. [<sup>11</sup>C]Pittsburgh compound B positron emission tomography and magnetic resonance brain scans were obtained in 149 participants including healthy controls and patients with subjective cognitive impairment, mild cognitive impairment and Alzheimer's disease. Magnetic resonance data were compared between high versus low-[11C]Pittsburgh compound B cases, and between high-[<sup>11</sup>C]Pittsburgh compound B cases with versus those without cognitive deficits. Larger temporal (including hippocampal) grey matter volume, associated with better episodic memory performance, was found in high- versus low-[<sup>11</sup>C]Pittsburgh compound B healthy controls. The same finding was obtained using different [<sup>11</sup>C]Pittsburgh compound B thresholds, correcting [<sup>11</sup>C]Pittsburgh compound B data for partial averaging, using age, education, Mini-Mental State Examination, apolipoprotein E4 and sex-matched subsamples, and using manual hippocampal delineation instead of voxel-based analysis. By contrast, in participants with subjective cognitive impairment, significant grey matter atrophy was found in high-[<sup>11</sup>C]Pittsburgh compound B cases compared to low-[<sup>11</sup>C]Pittsburgh compound B cases, as well as in high-[<sup>11</sup>C]Pittsburgh compound B cases with subjective cognitive impairment, mild cognitive impairment and Alzheimer's disease compared to high-[<sup>11</sup>C]Pittsburgh compound B healthy controls. Larger grey matter volume in high-[<sup>11</sup>C]Pittsburgh compound B healthy controls may reflect either a tissue reactive response to β-amyloid or a combination of higher 'brain reserve' and under-representation of subjects with standard/low temporal volume in the high-[<sup>11</sup>C]Pittsburgh compound B healthy controls. Our complementary analyses tend to support the latter hypotheses. Overall, our findings suggest that the deleterious effects of β-amyloid on cognition may be delayed in those subjects with larger brain (temporal) volume.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17</s0></fC02><fC02 i1="02" i2="X"><s0>002B17A03</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Démence d'Alzheimer</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Alzheimer disease</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Demencia Alzheimer</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Atrophie</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Atrophy</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Atrofia</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Personne âgée</s0><s5>09</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Elderly</s0><s5>09</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Anciano</s0><s5>09</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Etude comparative</s0><s5>10</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Comparative study</s0><s5>10</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Estudio comparativo</s0><s5>10</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Amyloïde</s0><s5>11</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Amyloid</s0><s5>11</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Amiloide</s0><s5>11</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Tomoscintigraphie</s0><s5>12</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Emission tomography</s0><s5>12</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Tomocentelleografía</s0><s5>12</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Tomographie par émission de positons</s0><s5>13</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Positron emission tomography</s0><s5>13</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Tomografía emisión positrones</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>347</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 10-0515981 INIST</NO><ET>Larger temporal volume in elderly with high versus low beta-amyloid deposition</ET><AU>CHETELAT (Gaël); VILLEMAGNE (Victor L.); PIKE (Kerryn E.); BARON (Jean-Claude); BOURGEAT (Pierrick); JONES (Gareth); FAUX (Noel G.); ELLIS (Kathryn A.); SALVADO (Olivier); SZOEKE (Cassandra); MARTINS (Ralph N.); AMES (David); MASTERS (Colin L.); ROWE (Christopher C.)</AU><AF>Department of Nuclear Medicine and Centre for PET, Austin Health/Heidelberg, VIC 3084/Australie (1 aut., 2 aut., 3 aut., 6 aut., 14 aut.); Inserm-EPHE-Université de Caen/Basse-Normandie, Unité U923, GIP Cyceron, CHU Côte de Nacre/14074 Caen/France (1 aut.); The Mental Health Research Institute, The University of Melbourne/Melbourne, VIC 3052/Australie (2 aut., 3 aut., 7 aut., 13 aut.); Department of Medicine, Austin Health, The University of Melbourne/Melbourne, VIC 3052/Australie (2 aut., 14 aut.); Department of Clinical Neurosciences, Neurology Unit, University of Cambridge/Cambridge CB2 2QQ/Royaume-Uni (4 aut.); CSIRO Preventative Health National Research Flagship ICTC, The Australian e-Health Research Centre, BioMedlA, Royal Brisbane and Women's Hospital/Herston, QLD 4006/Australie (5 aut., 9 aut.); Academic Unit for Psychiatry of Old Age, Department of Psychiatry, The University of Melbourne, St. Vincent's Aged Psychiatry Service, St George's Hospital/Melbourne VIC 3101/Australie (8 aut.); CSIRO Neurodegenerative Disease, Mental Disorders & Brain Health, Preventative Health Flagship, CSIRO Molecular and Health Technologies, Parkville/Melbourne, VIC 3052/Australie (10 aut.); Centre of Excellence for Alzheimer's Disease Research & Care, School of Exercise Biomedical and Health Sciences, Edith Cowan University/Joondalup, WA 6027/Australie (11 aut.); National Ageing Research Institute/Melbourne, VIC 3052/Australie (12 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>Brain; ISSN 0006-8950; Royaume-Uni; Da. 2010; Vol. 133; No. p. 11; Pp. 3349-3358; Bibl. 3/4 p.</SO><LA>Anglais</LA><EA>β-Amyloid deposition is one of the main hallmarks of Alzheimer's disease thought to eventually cause neuronal death. Post-mortem and neuroimaging studies have consistently reported cases with documented normal cognition despite high β-amylold burden. It is of great interest to understand what differentiates these particular subjects from those without β-amyloid deposition or with both β-amyloid deposition and cognitive deficits, i.e. what allows these subjects to resist the damage of the pathological lesions. [<sup>11</sup>C]Pittsburgh compound B positron emission tomography and magnetic resonance brain scans were obtained in 149 participants including healthy controls and patients with subjective cognitive impairment, mild cognitive impairment and Alzheimer's disease. Magnetic resonance data were compared between high versus low-[11C]Pittsburgh compound B cases, and between high-[<sup>11</sup>C]Pittsburgh compound B cases with versus those without cognitive deficits. Larger temporal (including hippocampal) grey matter volume, associated with better episodic memory performance, was found in high- versus low-[<sup>11</sup>C]Pittsburgh compound B healthy controls. The same finding was obtained using different [<sup>11</sup>C]Pittsburgh compound B thresholds, correcting [<sup>11</sup>C]Pittsburgh compound B data for partial averaging, using age, education, Mini-Mental State Examination, apolipoprotein E4 and sex-matched subsamples, and using manual hippocampal delineation instead of voxel-based analysis. By contrast, in participants with subjective cognitive impairment, significant grey matter atrophy was found in high-[<sup>11</sup>C]Pittsburgh compound B cases compared to low-[<sup>11</sup>C]Pittsburgh compound B cases, as well as in high-[<sup>11</sup>C]Pittsbur gh compound B cases with subjective cognitive impairment, mild cognitive impairment and Alzheimer's disease compared to high-[<sup>11</sup>C]Pittsburgh compound B healthy controls. Larger grey matter volume in high-[<sup>11</sup>C]Pittsburgh compound B healthy controls may reflect either a tissue reactive response to β-amyloid or a combination of higher 'brain reserve' and under-representation of subjects with standard/low temporal volume in the high-[<sup>11</sup>C]Pittsburgh compound B healthy controls. Our complementary analyses tend to support the latter hypotheses. Overall, our findings suggest that the deleterious effects of β-amyloid on cognition may be delayed in those subjects with larger brain (temporal) volume.</EA><CC>002B17; 002B17A03</CC><FD>Démence d'Alzheimer; Atrophie; Pathologie du système nerveux; Personne âgée; Etude comparative; Amyloïde; Tomoscintigraphie; Tomographie par émission de positons</FD><FG>Homme; Pathologie de l'encéphale; Maladie dégénérative; Pathologie du système nerveux central</FG><ED>Alzheimer disease; Atrophy; Nervous system diseases; Elderly; Comparative study; Amyloid; Emission tomography; Positron emission tomography</ED><EG>Human; Cerebral disorder; Degenerative disease; Central nervous system disease</EG><SD>Demencia Alzheimer; Atrofia; Sistema nervioso patología; Anciano; Estudio comparativo; Amiloide; Tomocentelleografía; Tomografía emisión positrones</SD><LO>INIST-998.354000193438630170</LO><ID>10-0515981</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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