AustralieFrV1, PascalFrancis, Corpus, bibRecord, 003850

Aβ deposits in older non-demented individuals with cognitive decline are indicative of preclinical Alzheimer's disease

Identifieur interne : 003850 ( PascalFrancis/Corpus ); précédent : 003849; suivant : 003851

Aβ deposits in older non-demented individuals with cognitive decline are indicative of preclinical Alzheimer's disease

Auteurs : V. L. Villemagne ; K. E. Pike ; D. Darby ; P. Maruff ; G. Savage ; S. Ng ; U. Ackermann ; T. F. Cowie ; J. Currie ; S. G. Chan ; G. Jones ; H. Tochon-Danguy ; G. O'Keefe ; C. L. Masters ; C. C. Rowe

Source :

Neuropsychologia [ 0028-3932 ] ; 2008.

RBID : Francis:08-0316070

Descripteurs français

Pascal (Inist)
- Détérioration intellectuelle, Trouble cognitif, Démence d'Alzheimer, Encéphale, Déficit cognitif léger, Amyloïde, Sénescence, Vieillissement, Tomoscintigraphie, Imagerie médicale, Facteur risque, Personne âgée.

English descriptors

KwdEn :
- Ageing, Alzheimer disease, Amyloid, Cognitive disorder, Elderly, Emission tomography, Encephalon, Intellectual deterioration, Medical imagery, Risk factor, Senescence, mild cognitive impairment.

Abstract

Approximately 30% of healthy persons aged over 75 years show Aβ deposition at autopsy. It is postulated that this represents preclinical Alzheimer's disease (AD). We evaluated the relationship between Aβ burden as assessed by PiB PET and cognitive decline in a well-characterized, non-demented, elderly cohort. PiB PET studies and cognitive tests were performed on 34 elderly participants (age 73 ± 6) from the longitudinal Melbourne Healthy Aging Study (MHAS). Subjects were classified as being cognitively 'stable' or 'declining' by an independent behavioural neurologist based on clinical assessment and serial word-list recall scores from the preceding 6-10 years. Decline was calculated from the slope of the word-list recall scores. Aβ burden was quantified using Standardized Uptake Value normalized to cerebellar cortex. Ten subjects were clinically classified as declining. At the time of the PET scans, three of the declining subjects had mild cognitive impairment, one had AD, and six were declining but remained within the normal range for age on cognitive tests. Declining subjects were much more likely to show cortical PiB binding than stable subjects (70% vs. 17%, respectively). Neocortical Aβ burden correlated with word-list recall slopes (r= -0.78) and memory function (r= -0.85) in the declining group. No correlations were observed in the stable group. Aβ burden correlated with incident memory impairment and the rate of memory decline in the non-demented ageing population. These observations suggest that neither memory decline nor Aβ deposition are part of normal ageing and likely represent preclinical AD. Further longitudinal observations are required to confirm this hypothesis.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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Format Inist (serveur)

NO :	FRANCIS 08-0316070 INIST
ET :	Aβ deposits in older non-demented individuals with cognitive decline are indicative of preclinical Alzheimer's disease
AU :	VILLEMAGNE (V. L.); PIKE (K. E.); DARBY (D.); MARUFF (P.); SAVAGE (G.); NG (S.); ACKERMANN (U.); COWIE (T. F.); CURRIE (J.); CHAN (S. G.); JONES (G.); TOCHON-DANGUY (H.); O'KEEFE (G.); MASTERS (C. L.); ROWE (C. C.); EUSTACHE (Francis); CHETELAT (Gaël)
AF :	Department of Nuclear Medicine, Centre for PET, Austin Health, 145 Studley Road/Heidelberg, VIC 3084/Australie (1 aut., 2 aut., 6 aut., 7 aut., 10 aut., 11 aut., 12 aut., 13 aut., 15 aut.); The Mental Health Research Institute of Victoria/Parkville, VIC/Australie (1 aut., 14 aut.); Department of Pathology, University of Melbourne/VIC/Australie (1 aut., 8 aut., 14 aut.); Centre for Neuroscience, University of Melbourne/VIC/Australie (1 aut., 3 aut., 4 aut., 14 aut.); School of Psychology, Psychiatry and Psychological Medicine, Monash University/Melbourne, VIC/Australie (2 aut., 5 aut.); Cogstate Pty Ltd/Melbourne, VIC/Australie (3 aut., 4 aut.); St Vincent's Hospital/Melbourne, VIC/Australie (9 aut.); Department of Medicine, (Austin Health) University of Melbourne/VIC/Australie (15 aut.); INSERM - EPHE - Université de Caen Basse Normandie, Unité de Recherche U923, Centre Cyceron, Bd H. Becquerel, BP 5229/14074 Caen/France (2 aut.); INSERM - EPHE - Université de Caen Basse Normandie, Unité de Recherche U923, "Neuropsychologie Cognitive et Neuroanatomie Fonctionnelle de la Mémoire Humaine", Laboratoire de Neuropsychologie, CHU, Avenue de la Côte de Nacre/14033 Caen/France (1 aut.)
DT :	Publication en série; Niveau analytique
SO :	Neuropsychologia; ISSN 0028-3932; Coden NUPSA6; Royaume-Uni; Da. 2008; Vol. 46; No. 6; Pp. 1688-1697; Bibl. 2 p.1/2
LA :	Anglais
EA :	Approximately 30% of healthy persons aged over 75 years show Aβ deposition at autopsy. It is postulated that this represents preclinical Alzheimer's disease (AD). We evaluated the relationship between Aβ burden as assessed by PiB PET and cognitive decline in a well-characterized, non-demented, elderly cohort. PiB PET studies and cognitive tests were performed on 34 elderly participants (age 73 ± 6) from the longitudinal Melbourne Healthy Aging Study (MHAS). Subjects were classified as being cognitively 'stable' or 'declining' by an independent behavioural neurologist based on clinical assessment and serial word-list recall scores from the preceding 6-10 years. Decline was calculated from the slope of the word-list recall scores. Aβ burden was quantified using Standardized Uptake Value normalized to cerebellar cortex. Ten subjects were clinically classified as declining. At the time of the PET scans, three of the declining subjects had mild cognitive impairment, one had AD, and six were declining but remained within the normal range for age on cognitive tests. Declining subjects were much more likely to show cortical PiB binding than stable subjects (70% vs. 17%, respectively). Neocortical Aβ burden correlated with word-list recall slopes (r= -0.78) and memory function (r= -0.85) in the declining group. No correlations were observed in the stable group. Aβ burden correlated with incident memory impairment and the rate of memory decline in the non-demented ageing population. These observations suggest that neither memory decline nor Aβ deposition are part of normal ageing and likely represent preclinical AD. Further longitudinal observations are required to confirm this hypothesis.
CC :	770D03M; 770D05
FD :	Détérioration intellectuelle; Trouble cognitif; Démence d'Alzheimer; Encéphale; Déficit cognitif léger; Amyloïde; Sénescence; Vieillissement; Tomoscintigraphie; Imagerie médicale; Facteur risque; Personne âgée
FG :	Homme; Pathologie de l'encéphale; Maladie dégénérative; Pathologie du système nerveux central; Pathologie du système nerveux; Système nerveux central
ED :	Intellectual deterioration; Cognitive disorder; Alzheimer disease; Encephalon; mild cognitive impairment; Amyloid; Senescence; Ageing; Emission tomography; Medical imagery; Risk factor; Elderly
EG :	Human; Cerebral disorder; Degenerative disease; Central nervous system disease; Nervous system diseases; Central nervous system
SD :	Deterioro intelectual; Trastorno cognitivo; Demencia Alzheimer; Encéfalo; Disturbio cognitivo ligero; Amiloide; Senescencia; Envejecimiento; Tomocentelleografía; Imaginería médica; Factor riesgo; Anciano
LO :	INIST-11143.354000197948670100
ID :	08-0316070

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Francis:08-0316070

Le document en format XML

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<author><name sortKey="Jones, G" sort="Jones, G" uniqKey="Jones G" first="G." last="Jones">G. Jones</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Nuclear Medicine, Centre for PET, Austin Health, 145 Studley Road</s1>
<s2>Heidelberg, VIC 3084</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
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</author>
<author><name sortKey="Tochon Danguy, H" sort="Tochon Danguy, H" uniqKey="Tochon Danguy H" first="H." last="Tochon-Danguy">H. Tochon-Danguy</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Nuclear Medicine, Centre for PET, Austin Health, 145 Studley Road</s1>
<s2>Heidelberg, VIC 3084</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
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</author>
<author><name sortKey="O Keefe, G" sort="O Keefe, G" uniqKey="O Keefe G" first="G." last="O'Keefe">G. O'Keefe</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Nuclear Medicine, Centre for PET, Austin Health, 145 Studley Road</s1>
<s2>Heidelberg, VIC 3084</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
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</author>
<author><name sortKey="Masters, C L" sort="Masters, C L" uniqKey="Masters C" first="C. L." last="Masters">C. L. Masters</name>
<affiliation><inist:fA14 i1="02"><s1>The Mental Health Research Institute of Victoria</s1>
<s2>Parkville, VIC</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>14 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="03"><s1>Department of Pathology, University of Melbourne</s1>
<s2>VIC</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>14 aut.</sZ>
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</affiliation>
<affiliation><inist:fA14 i1="04"><s1>Centre for Neuroscience, University of Melbourne</s1>
<s2>VIC</s2>
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<sZ>1 aut.</sZ>
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<sZ>4 aut.</sZ>
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</affiliation>
</author>
<author><name sortKey="Rowe, C C" sort="Rowe, C C" uniqKey="Rowe C" first="C. C." last="Rowe">C. C. Rowe</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Nuclear Medicine, Centre for PET, Austin Health, 145 Studley Road</s1>
<s2>Heidelberg, VIC 3084</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
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<sZ>12 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>15 aut.</sZ>
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</affiliation>
<affiliation><inist:fA14 i1="08"><s1>Department of Medicine, (Austin Health) University of Melbourne</s1>
<s2>VIC</s2>
<s3>AUS</s3>
<sZ>15 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">08-0316070</idno>
<date when="2008">2008</date>
<idno type="stanalyst">FRANCIS 08-0316070 INIST</idno>
<idno type="RBID">Francis:08-0316070</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">003850</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Aβ deposits in older non-demented individuals with cognitive decline are indicative of preclinical Alzheimer's disease</title>
<author><name sortKey="Villemagne, V L" sort="Villemagne, V L" uniqKey="Villemagne V" first="V. L." last="Villemagne">V. L. Villemagne</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Nuclear Medicine, Centre for PET, Austin Health, 145 Studley Road</s1>
<s2>Heidelberg, VIC 3084</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>15 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>The Mental Health Research Institute of Victoria</s1>
<s2>Parkville, VIC</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>14 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="03"><s1>Department of Pathology, University of Melbourne</s1>
<s2>VIC</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>14 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="04"><s1>Centre for Neuroscience, University of Melbourne</s1>
<s2>VIC</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>14 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Pike, K E" sort="Pike, K E" uniqKey="Pike K" first="K. E." last="Pike">K. E. Pike</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Nuclear Medicine, Centre for PET, Austin Health, 145 Studley Road</s1>
<s2>Heidelberg, VIC 3084</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>15 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="05"><s1>School of Psychology, Psychiatry and Psychological Medicine, Monash University</s1>
<s2>Melbourne, VIC</s2>
<s3>AUS</s3>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Darby, D" sort="Darby, D" uniqKey="Darby D" first="D." last="Darby">D. Darby</name>
<affiliation><inist:fA14 i1="04"><s1>Centre for Neuroscience, University of Melbourne</s1>
<s2>VIC</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>14 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="06"><s1>Cogstate Pty Ltd</s1>
<s2>Melbourne, VIC</s2>
<s3>AUS</s3>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Maruff, P" sort="Maruff, P" uniqKey="Maruff P" first="P." last="Maruff">P. Maruff</name>
<affiliation><inist:fA14 i1="04"><s1>Centre for Neuroscience, University of Melbourne</s1>
<s2>VIC</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
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</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="06"><s1>Cogstate Pty Ltd</s1>
<s2>Melbourne, VIC</s2>
<s3>AUS</s3>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Savage, G" sort="Savage, G" uniqKey="Savage G" first="G." last="Savage">G. Savage</name>
<affiliation><inist:fA14 i1="05"><s1>School of Psychology, Psychiatry and Psychological Medicine, Monash University</s1>
<s2>Melbourne, VIC</s2>
<s3>AUS</s3>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Ng, S" sort="Ng, S" uniqKey="Ng S" first="S." last="Ng">S. Ng</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Nuclear Medicine, Centre for PET, Austin Health, 145 Studley Road</s1>
<s2>Heidelberg, VIC 3084</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>15 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Ackermann, U" sort="Ackermann, U" uniqKey="Ackermann U" first="U." last="Ackermann">U. Ackermann</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Nuclear Medicine, Centre for PET, Austin Health, 145 Studley Road</s1>
<s2>Heidelberg, VIC 3084</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>15 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Cowie, T F" sort="Cowie, T F" uniqKey="Cowie T" first="T. F." last="Cowie">T. F. Cowie</name>
<affiliation><inist:fA14 i1="03"><s1>Department of Pathology, University of Melbourne</s1>
<s2>VIC</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>14 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Currie, J" sort="Currie, J" uniqKey="Currie J" first="J." last="Currie">J. Currie</name>
<affiliation><inist:fA14 i1="07"><s1>St Vincent's Hospital</s1>
<s2>Melbourne, VIC</s2>
<s3>AUS</s3>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Chan, S G" sort="Chan, S G" uniqKey="Chan S" first="S. G." last="Chan">S. G. Chan</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Nuclear Medicine, Centre for PET, Austin Health, 145 Studley Road</s1>
<s2>Heidelberg, VIC 3084</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>15 aut.</sZ>
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</affiliation>
</author>
<author><name sortKey="Jones, G" sort="Jones, G" uniqKey="Jones G" first="G." last="Jones">G. Jones</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Nuclear Medicine, Centre for PET, Austin Health, 145 Studley Road</s1>
<s2>Heidelberg, VIC 3084</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>15 aut.</sZ>
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</affiliation>
</author>
<author><name sortKey="Tochon Danguy, H" sort="Tochon Danguy, H" uniqKey="Tochon Danguy H" first="H." last="Tochon-Danguy">H. Tochon-Danguy</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Nuclear Medicine, Centre for PET, Austin Health, 145 Studley Road</s1>
<s2>Heidelberg, VIC 3084</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>15 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="O Keefe, G" sort="O Keefe, G" uniqKey="O Keefe G" first="G." last="O'Keefe">G. O'Keefe</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Nuclear Medicine, Centre for PET, Austin Health, 145 Studley Road</s1>
<s2>Heidelberg, VIC 3084</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>15 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Masters, C L" sort="Masters, C L" uniqKey="Masters C" first="C. L." last="Masters">C. L. Masters</name>
<affiliation><inist:fA14 i1="02"><s1>The Mental Health Research Institute of Victoria</s1>
<s2>Parkville, VIC</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>14 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="03"><s1>Department of Pathology, University of Melbourne</s1>
<s2>VIC</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>14 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="04"><s1>Centre for Neuroscience, University of Melbourne</s1>
<s2>VIC</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
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</affiliation>
</author>
<author><name sortKey="Rowe, C C" sort="Rowe, C C" uniqKey="Rowe C" first="C. C." last="Rowe">C. C. Rowe</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Nuclear Medicine, Centre for PET, Austin Health, 145 Studley Road</s1>
<s2>Heidelberg, VIC 3084</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
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<sZ>12 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>15 aut.</sZ>
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</affiliation>
<affiliation><inist:fA14 i1="08"><s1>Department of Medicine, (Austin Health) University of Melbourne</s1>
<s2>VIC</s2>
<s3>AUS</s3>
<sZ>15 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">Neuropsychologia</title>
<title level="j" type="abbreviated">Neuropsychologia</title>
<idno type="ISSN">0028-3932</idno>
<imprint><date when="2008">2008</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Neuropsychologia</title>
<title level="j" type="abbreviated">Neuropsychologia</title>
<idno type="ISSN">0028-3932</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Ageing</term>
<term>Alzheimer disease</term>
<term>Amyloid</term>
<term>Cognitive disorder</term>
<term>Elderly</term>
<term>Emission tomography</term>
<term>Encephalon</term>
<term>Intellectual deterioration</term>
<term>Medical imagery</term>
<term>Risk factor</term>
<term>Senescence</term>
<term>mild cognitive impairment</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Détérioration intellectuelle</term>
<term>Trouble cognitif</term>
<term>Démence d'Alzheimer</term>
<term>Encéphale</term>
<term>Déficit cognitif léger</term>
<term>Amyloïde</term>
<term>Sénescence</term>
<term>Vieillissement</term>
<term>Tomoscintigraphie</term>
<term>Imagerie médicale</term>
<term>Facteur risque</term>
<term>Personne âgée</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Approximately 30% of healthy persons aged over 75 years show Aβ deposition at autopsy. It is postulated that this represents preclinical Alzheimer's disease (AD). We evaluated the relationship between Aβ burden as assessed by PiB PET and cognitive decline in a well-characterized, non-demented, elderly cohort. PiB PET studies and cognitive tests were performed on 34 elderly participants (age 73 ± 6) from the longitudinal Melbourne Healthy Aging Study (MHAS). Subjects were classified as being cognitively 'stable' or 'declining' by an independent behavioural neurologist based on clinical assessment and serial word-list recall scores from the preceding 6-10 years. Decline was calculated from the slope of the word-list recall scores. Aβ burden was quantified using Standardized Uptake Value normalized to cerebellar cortex. Ten subjects were clinically classified as declining. At the time of the PET scans, three of the declining subjects had mild cognitive impairment, one had AD, and six were declining but remained within the normal range for age on cognitive tests. Declining subjects were much more likely to show cortical PiB binding than stable subjects (70% vs. 17%, respectively). Neocortical Aβ burden correlated with word-list recall slopes (r= -0.78) and memory function (r= -0.85) in the declining group. No correlations were observed in the stable group. Aβ burden correlated with incident memory impairment and the rate of memory decline in the non-demented ageing population. These observations suggest that neither memory decline nor Aβ deposition are part of normal ageing and likely represent preclinical AD. Further longitudinal observations are required to confirm this hypothesis.</div>
</front>
</TEI>
<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0028-3932</s0>
</fA01>
<fA02 i1="01"><s0>NUPSA6</s0>
</fA02>
<fA03 i2="1"><s0>Neuropsychologia</s0>
</fA03>
<fA05><s2>46</s2>
</fA05>
<fA06><s2>6</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Aβ deposits in older non-demented individuals with cognitive decline are indicative of preclinical Alzheimer's disease</s1>
</fA08>
<fA09 i1="01" i2="1" l="ENG"><s1>Neuroimaging of Early Alzheimer's Disease</s1>
</fA09>
<fA11 i1="01" i2="1"><s1>VILLEMAGNE (V. L.)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>PIKE (K. E.)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>DARBY (D.)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>MARUFF (P.)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>SAVAGE (G.)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>NG (S.)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>ACKERMANN (U.)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>COWIE (T. F.)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>CURRIE (J.)</s1>
</fA11>
<fA11 i1="10" i2="1"><s1>CHAN (S. G.)</s1>
</fA11>
<fA11 i1="11" i2="1"><s1>JONES (G.)</s1>
</fA11>
<fA11 i1="12" i2="1"><s1>TOCHON-DANGUY (H.)</s1>
</fA11>
<fA11 i1="13" i2="1"><s1>O'KEEFE (G.)</s1>
</fA11>
<fA11 i1="14" i2="1"><s1>MASTERS (C. L.)</s1>
</fA11>
<fA11 i1="15" i2="1"><s1>ROWE (C. C.)</s1>
</fA11>
<fA12 i1="01" i2="1"><s1>EUSTACHE (Francis)</s1>
<s9>ed.</s9>
</fA12>
<fA12 i1="02" i2="1"><s1>CHETELAT (Gaël)</s1>
<s9>ed.</s9>
</fA12>
<fA14 i1="01"><s1>Department of Nuclear Medicine, Centre for PET, Austin Health, 145 Studley Road</s1>
<s2>Heidelberg, VIC 3084</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>15 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>The Mental Health Research Institute of Victoria</s1>
<s2>Parkville, VIC</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>14 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Pathology, University of Melbourne</s1>
<s2>VIC</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>14 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Centre for Neuroscience, University of Melbourne</s1>
<s2>VIC</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>14 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>School of Psychology, Psychiatry and Psychological Medicine, Monash University</s1>
<s2>Melbourne, VIC</s2>
<s3>AUS</s3>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Cogstate Pty Ltd</s1>
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<server><NO>FRANCIS 08-0316070 INIST</NO>
<ET>Aβ deposits in older non-demented individuals with cognitive decline are indicative of preclinical Alzheimer's disease</ET>
<AU>VILLEMAGNE (V. L.); PIKE (K. E.); DARBY (D.); MARUFF (P.); SAVAGE (G.); NG (S.); ACKERMANN (U.); COWIE (T. F.); CURRIE (J.); CHAN (S. G.); JONES (G.); TOCHON-DANGUY (H.); O'KEEFE (G.); MASTERS (C. L.); ROWE (C. C.); EUSTACHE (Francis); CHETELAT (Gaël)</AU>
<AF>Department of Nuclear Medicine, Centre for PET, Austin Health, 145 Studley Road/Heidelberg, VIC 3084/Australie (1 aut., 2 aut., 6 aut., 7 aut., 10 aut., 11 aut., 12 aut., 13 aut., 15 aut.); The Mental Health Research Institute of Victoria/Parkville, VIC/Australie (1 aut., 14 aut.); Department of Pathology, University of Melbourne/VIC/Australie (1 aut., 8 aut., 14 aut.); Centre for Neuroscience, University of Melbourne/VIC/Australie (1 aut., 3 aut., 4 aut., 14 aut.); School of Psychology, Psychiatry and Psychological Medicine, Monash University/Melbourne, VIC/Australie (2 aut., 5 aut.); Cogstate Pty Ltd/Melbourne, VIC/Australie (3 aut., 4 aut.); St Vincent's Hospital/Melbourne, VIC/Australie (9 aut.); Department of Medicine, (Austin Health) University of Melbourne/VIC/Australie (15 aut.); INSERM - EPHE - Université de Caen Basse Normandie, Unité de Recherche U923, Centre Cyceron, Bd H. Becquerel, BP 5229/14074 Caen/France (2 aut.); INSERM - EPHE - Université de Caen Basse Normandie, Unité de Recherche U923, "Neuropsychologie Cognitive et Neuroanatomie Fonctionnelle de la Mémoire Humaine", Laboratoire de Neuropsychologie, CHU, Avenue de la Côte de Nacre/14033 Caen/France (1 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Neuropsychologia; ISSN 0028-3932; Coden NUPSA6; Royaume-Uni; Da. 2008; Vol. 46; No. 6; Pp. 1688-1697; Bibl. 2 p.1/2</SO>
<LA>Anglais</LA>
<EA>Approximately 30% of healthy persons aged over 75 years show Aβ deposition at autopsy. It is postulated that this represents preclinical Alzheimer's disease (AD). We evaluated the relationship between Aβ burden as assessed by PiB PET and cognitive decline in a well-characterized, non-demented, elderly cohort. PiB PET studies and cognitive tests were performed on 34 elderly participants (age 73 ± 6) from the longitudinal Melbourne Healthy Aging Study (MHAS). Subjects were classified as being cognitively 'stable' or 'declining' by an independent behavioural neurologist based on clinical assessment and serial word-list recall scores from the preceding 6-10 years. Decline was calculated from the slope of the word-list recall scores. Aβ burden was quantified using Standardized Uptake Value normalized to cerebellar cortex. Ten subjects were clinically classified as declining. At the time of the PET scans, three of the declining subjects had mild cognitive impairment, one had AD, and six were declining but remained within the normal range for age on cognitive tests. Declining subjects were much more likely to show cortical PiB binding than stable subjects (70% vs. 17%, respectively). Neocortical Aβ burden correlated with word-list recall slopes (r= -0.78) and memory function (r= -0.85) in the declining group. No correlations were observed in the stable group. Aβ burden correlated with incident memory impairment and the rate of memory decline in the non-demented ageing population. These observations suggest that neither memory decline nor Aβ deposition are part of normal ageing and likely represent preclinical AD. Further longitudinal observations are required to confirm this hypothesis.</EA>
<CC>770D03M; 770D05</CC>
<FD>Détérioration intellectuelle; Trouble cognitif; Démence d'Alzheimer; Encéphale; Déficit cognitif léger; Amyloïde; Sénescence; Vieillissement; Tomoscintigraphie; Imagerie médicale; Facteur risque; Personne âgée</FD>
<FG>Homme; Pathologie de l'encéphale; Maladie dégénérative; Pathologie du   système nerveux central; Pathologie du   système nerveux; Système nerveux central</FG>
<ED>Intellectual deterioration; Cognitive disorder; Alzheimer disease; Encephalon; mild cognitive impairment; Amyloid; Senescence; Ageing; Emission tomography; Medical imagery; Risk factor; Elderly</ED>
<EG>Human; Cerebral disorder; Degenerative disease; Central nervous system disease; Nervous system diseases; Central nervous system</EG>
<SD>Deterioro intelectual; Trastorno cognitivo; Demencia Alzheimer; Encéfalo; Disturbio cognitivo ligero; Amiloide; Senescencia; Envejecimiento; Tomocentelleografía; Imaginería médica; Factor riesgo; Anciano</SD>
<LO>INIST-11143.354000197948670100</LO>
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Aβ deposits in older non-demented individuals with cognitive decline are indicative of preclinical Alzheimer's disease

Aβ deposits in older non-demented individuals with cognitive decline are indicative of preclinical Alzheimer's disease

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