Larger temporal volume in elderly with high versus low beta-amyloid deposition
Identifieur interne : 007088 ( Main/Exploration ); précédent : 007087; suivant : 007089Larger temporal volume in elderly with high versus low beta-amyloid deposition
Auteurs : Gaël Chételat [Australie, France] ; Victor L. Villemagne [Australie] ; Kerryn E. Pike [Australie] ; Jean-Claude Baron [Royaume-Uni] ; Pierrick Bourgeat [Australie] ; Gareth Jones [Australie] ; Noel G. Faux [Australie] ; Kathryn A. Ellis [Australie] ; Olivier Salvado [Australie] ; Cassandra Szoeke [Australie] ; Ralph N. Martins [Australie] ; David Ames [Australie] ; Colin L. Masters [Australie] ; Christopher C. Rowe [Australie]Source :
- Brain [ 0006-8950 ] ; 2010-11.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Personne âgée.
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-amyloid 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.
Url:
DOI: 10.1093/brain/awq187
Affiliations:
- Australie, France, Royaume-Uni
- Angleterre, Angleterre de l'Est, Basse-Normandie, Région Normandie, Victoria (État)
- Caen, Cambridge, Melbourne
- Université de Cambridge, Université de Melbourne
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Ellis</name><affiliation wicri:level="4"><country xml:lang="fr">Australie</country><wicri:regionArea>7 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</wicri:regionArea><orgName type="university">Université de Melbourne</orgName><placeName><settlement type="city">Melbourne</settlement><region type="état">Victoria (État)</region></placeName></affiliation></author><author><name sortKey="Salvado, Olivier" sort="Salvado, Olivier" uniqKey="Salvado O" first="Olivier" last="Salvado">Olivier Salvado</name><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>6 CSIRO Preventative Health National Research Flagship ICTC, The Australian e-Health Research Centre, BioMedIA, Royal Brisbane and Women's Hospital, Herston, QLD 4006</wicri:regionArea><wicri:noRegion>QLD 4006</wicri:noRegion></affiliation></author><author><name sortKey="Szoeke, Cassandra" sort="Szoeke, Cassandra" uniqKey="Szoeke C" first="Cassandra" last="Szoeke">Cassandra Szoeke</name><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>8 CSIRO Neurodegenerative Disease, Mental Disorders & Brain Health, Preventative Health Flagship, CSIRO Molecular and Health Technologies, Parkville, Melbourne, VIC 3052</wicri:regionArea><wicri:noRegion>VIC 3052</wicri:noRegion></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"><country xml:lang="fr">Australie</country><wicri:regionArea>9 Centre of Excellence for Alzheimer’s Disease Research & Care, School of Exercise Biomedical and Health Sciences, Edith Cowan University, Joondalup, WA 6027</wicri:regionArea><wicri:noRegion>WA 6027</wicri:noRegion></affiliation></author><author><name sortKey="Ames, David" sort="Ames, David" uniqKey="Ames D" first="David" last="Ames">David Ames</name><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>10 National Ageing Research Institute, Melbourne, VIC 3052</wicri:regionArea><wicri:noRegion>VIC 3052</wicri:noRegion></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="4"><country xml:lang="fr">Australie</country><wicri:regionArea>3 The Mental Health Research Institute, The University of Melbourne, Melbourne, VIC 3052</wicri:regionArea><orgName type="university">Université de Melbourne</orgName><placeName><settlement type="city">Melbourne</settlement><region type="état">Victoria (État)</region></placeName></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"><country xml:lang="fr">Australie</country><wicri:regionArea>1 Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, VIC 3084</wicri:regionArea><wicri:noRegion>VIC 3084</wicri:noRegion></affiliation><affiliation wicri:level="4"><country xml:lang="fr">Australie</country><wicri:regionArea>4 Department of Medicine, Austin Health, The University of Melbourne, Melbourne, VIC 3052</wicri:regionArea><orgName type="university">Université de Melbourne</orgName><placeName><settlement type="city">Melbourne</settlement><region type="état">Victoria (État)</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain</title><idno type="ISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2010-11">2010-11</date><biblScope unit="volume">133</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="3349">3349</biblScope><biblScope unit="page" to="3358">3358</biblScope></imprint><idno type="ISSN">0006-8950</idno></series></biblStruct></sourceDesc><seriesStmt><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>Amyloïde</term><term>Atrophie</term><term>Démence d'Alzheimer</term><term>Etude comparative</term><term>Pathologie du système nerveux</term><term>Personne âgée</term><term>Tomographie par émission de positons</term><term>Tomoscintigraphie</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Personne âgée</term></keywords></textClass></profileDesc></teiHeader><front><div type="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-amyloid 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.</div></front></TEI><affiliations><list><country><li>Australie</li><li>France</li><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Angleterre de l'Est</li><li>Basse-Normandie</li><li>Région Normandie</li><li>Victoria (État)</li></region><settlement><li>Caen</li><li>Cambridge</li><li>Melbourne</li></settlement><orgName><li>Université de Cambridge</li><li>Université de Melbourne</li></orgName></list><tree><country name="Australie"><noRegion><name sortKey="Chetelat, Gael" sort="Chetelat, Gael" uniqKey="Chetelat G" first="Gaël" last="Chételat">Gaël Chételat</name></noRegion><name sortKey="Ames, David" sort="Ames, David" uniqKey="Ames D" first="David" last="Ames">David Ames</name><name sortKey="Bourgeat, Pierrick" sort="Bourgeat, Pierrick" uniqKey="Bourgeat P" first="Pierrick" last="Bourgeat">Pierrick Bourgeat</name><name sortKey="Ellis, Kathryn A" sort="Ellis, Kathryn A" uniqKey="Ellis K" first="Kathryn A." last="Ellis">Kathryn A. Ellis</name><name sortKey="Faux, Noel G" sort="Faux, Noel G" uniqKey="Faux N" first="Noel G." last="Faux">Noel G. Faux</name><name sortKey="Jones, Gareth" sort="Jones, Gareth" uniqKey="Jones G" first="Gareth" last="Jones">Gareth Jones</name><name sortKey="Martins, Ralph N" sort="Martins, Ralph N" uniqKey="Martins R" first="Ralph N." last="Martins">Ralph N. Martins</name><name sortKey="Masters, Colin L" sort="Masters, Colin L" uniqKey="Masters C" first="Colin L." last="Masters">Colin L. Masters</name><name sortKey="Pike, Kerryn E" sort="Pike, Kerryn E" uniqKey="Pike K" first="Kerryn E." last="Pike">Kerryn E. Pike</name><name sortKey="Pike, Kerryn E" sort="Pike, Kerryn E" uniqKey="Pike K" first="Kerryn E." last="Pike">Kerryn E. Pike</name><name sortKey="Rowe, Christopher C" sort="Rowe, Christopher C" uniqKey="Rowe C" first="Christopher C." last="Rowe">Christopher C. Rowe</name><name sortKey="Rowe, Christopher C" sort="Rowe, Christopher C" uniqKey="Rowe C" first="Christopher C." last="Rowe">Christopher C. Rowe</name><name sortKey="Salvado, Olivier" sort="Salvado, Olivier" uniqKey="Salvado O" first="Olivier" last="Salvado">Olivier Salvado</name><name sortKey="Szoeke, Cassandra" sort="Szoeke, Cassandra" uniqKey="Szoeke C" first="Cassandra" last="Szoeke">Cassandra Szoeke</name><name sortKey="Villemagne, Victor L" sort="Villemagne, Victor L" uniqKey="Villemagne V" first="Victor L." last="Villemagne">Victor L. Villemagne</name><name sortKey="Villemagne, Victor L" sort="Villemagne, Victor L" uniqKey="Villemagne V" first="Victor L." last="Villemagne">Victor L. Villemagne</name><name sortKey="Villemagne, Victor L" sort="Villemagne, Victor L" uniqKey="Villemagne V" first="Victor L." last="Villemagne">Victor L. Villemagne</name></country><country name="France"><region name="Région Normandie"><name sortKey="Chetelat, Gael" sort="Chetelat, Gael" uniqKey="Chetelat G" first="Gaël" last="Chételat">Gaël Chételat</name></region><name sortKey="Chetelat, Gael" sort="Chetelat, Gael" uniqKey="Chetelat G" first="Gaël" last="Chételat">Gaël Chételat</name></country><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Baron, Jean Claude" sort="Baron, Jean Claude" uniqKey="Baron J" first="Jean-Claude" last="Baron">Jean-Claude Baron</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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