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000270307 037__ $$aDZNE-2024-00779
000270307 041__ $$aEnglish
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000270307 1001_ $$aQuenon, Lisa$$b0
000270307 245__ $$aAmyloid-PET imaging predicts functional decline in clinically normal individuals.
000270307 260__ $$aLondon$$bBioMed Central$$c2024
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000270307 520__ $$aThere is good evidence that elevated amyloid-β (Aβ) positron emission tomography (PET) signal is associated with cognitive decline in clinically normal (CN) individuals. However, it is less well established whether there is an association between the Aβ burden and decline in daily living activities in this population. Moreover, Aβ-PET Centiloids (CL) thresholds that can optimally predict functional decline have not yet been established.Cross-sectional and longitudinal analyses over a mean three-year timeframe were performed on the European amyloid-PET imaging AMYPAD-PNHS dataset that phenotypes 1260 individuals, including 1032 CN individuals and 228 participants with questionable functional impairment. Amyloid-PET was assessed continuously on the Centiloid (CL) scale and using Aβ groups (CL < 12 = Aβ-, 12 ≤ CL ≤ 50 = Aβ-intermediate/Aβ± , CL > 50 = Aβ+). Functional abilities were longitudinally assessed using the Clinical Dementia Rating (Global-CDR, CDR-SOB) and the Amsterdam Instrumental Activities of Daily Living Questionnaire (A-IADL-Q). The Global-CDR was available for the 1260 participants at baseline, while baseline CDR-SOB and A-IADL-Q scores and longitudinal functional data were available for different subsamples that had similar characteristics to those of the entire sample.Participants included 765 Aβ- (61%, Mdnage = 66.0, IQRage = 61.0-71.0; 59% women), 301 Aβ± (24%; Mdnage = 69.0, IQRage = 64.0-75.0; 53% women) and 194 Aβ+ individuals (15%, Mdnage = 73.0, IQRage = 68.0-78.0; 53% women). Cross-sectionally, CL values were associated with CDR outcomes. Longitudinally, baseline CL values predicted prospective changes in the CDR-SOB (bCL*Time = 0.001/CL/year, 95% CI [0.0005,0.0024], p = .003) and A-IADL-Q (bCL*Time = -0.010/CL/year, 95% CI [-0.016,-0.004], p = .002) scores in initially CN participants. Increased clinical progression (Global-CDR > 0) was mainly observed in Aβ+ CN individuals (HRAβ+ vs Aβ- = 2.55, 95% CI [1.16,5.60], p = .020). Optimal thresholds for predicting decline were found at 41 CL using the CDR-SOB (bAβ+ vs Aβ- = 0.137/year, 95% CI [0.069,0.206], p < .001) and 28 CL using the A-IADL-Q (bAβ+ vs Aβ- = -0.693/year, 95% CI [-1.179,-0.208], p = .005).Amyloid-PET quantification supports the identification of CN individuals at risk of functional decline.The AMYPAD PNHS is registered at www.clinicaltrialsregister.eu with the EudraCT Number: 2018-002277-22.
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000270307 650_7 $$2Other$$aAmyloid-PET
000270307 650_7 $$2Other$$aCentiloid
000270307 650_7 $$2Other$$aFunctional decline
000270307 650_7 $$2Other$$aInstrumental activities of daily living
000270307 650_7 $$2Other$$aPreclinical Alzheimer
000270307 650_7 $$2NLM Chemicals$$aAmyloid beta-Peptides
000270307 650_2 $$2MeSH$$aHumans
000270307 650_2 $$2MeSH$$aPositron-Emission Tomography: methods
000270307 650_2 $$2MeSH$$aFemale
000270307 650_2 $$2MeSH$$aMale
000270307 650_2 $$2MeSH$$aCross-Sectional Studies
000270307 650_2 $$2MeSH$$aLongitudinal Studies
000270307 650_2 $$2MeSH$$aAged
000270307 650_2 $$2MeSH$$aAmyloid beta-Peptides: metabolism
000270307 650_2 $$2MeSH$$aActivities of Daily Living
000270307 650_2 $$2MeSH$$aCognitive Dysfunction: diagnostic imaging
000270307 650_2 $$2MeSH$$aCognitive Dysfunction: metabolism
000270307 650_2 $$2MeSH$$aMiddle Aged
000270307 650_2 $$2MeSH$$aBrain: diagnostic imaging
000270307 650_2 $$2MeSH$$aBrain: metabolism
000270307 650_2 $$2MeSH$$aAged, 80 and over
000270307 7001_ $$aCollij, Lyduine E$$b1
000270307 7001_ $$aGarcia, David Vállez$$b2
000270307 7001_ $$aLopes Alves, Isadora$$b3
000270307 7001_ $$aGérard, Thomas$$b4
000270307 7001_ $$aMalotaux, Vincent$$b5
000270307 7001_ $$aHuyghe, Lara$$b6
000270307 7001_ $$aGispert, Juan Domingo$$b7
000270307 7001_ $$0P:(DE-2719)2000032$$aJessen, Frank$$b8$$udzne
000270307 7001_ $$aVisser, Pieter Jelle$$b9
000270307 7001_ $$aden Braber, Anouk$$b10
000270307 7001_ $$aRitchie, Craig W$$b11
000270307 7001_ $$aBoada, Mercè$$b12
000270307 7001_ $$aMarquié, Marta$$b13
000270307 7001_ $$aVandenberghe, Rik$$b14
000270307 7001_ $$aLuckett, Emma S$$b15
000270307 7001_ $$aSchöll, Michael$$b16
000270307 7001_ $$aFrisoni, Giovanni B$$b17
000270307 7001_ $$aBuckley, Christopher$$b18
000270307 7001_ $$aStephens, Andrew$$b19
000270307 7001_ $$aAltomare, Daniele$$b20
000270307 7001_ $$aFord, Lisa$$b21
000270307 7001_ $$aBirck, Cindy$$b22
000270307 7001_ $$aMett, Anja$$b23
000270307 7001_ $$aGismondi, Rossella$$b24
000270307 7001_ $$aWolz, Robin$$b25
000270307 7001_ $$aGrootoonk, Sylke$$b26
000270307 7001_ $$aManber, Richard$$b27
000270307 7001_ $$aShekari, Mahnaz$$b28
000270307 7001_ $$aLhommel, Renaud$$b29
000270307 7001_ $$aDricot, Laurence$$b30
000270307 7001_ $$aIvanoiu, Adrian$$b31
000270307 7001_ $$aFarrar, Gill$$b32
000270307 7001_ $$aBarkhof, Frederik$$b33
000270307 7001_ $$aHanseeuw, Bernard J$$b34
000270307 7001_ $$aConsortium, AMYPAD$$b35$$eCollaboration Author
000270307 773__ $$0PERI:(DE-600)2506521-X$$a10.1186/s13195-024-01494-9$$gVol. 16, no. 1, p. 130$$n1$$p130$$tAlzheimer's research & therapy$$v16$$x1758-9193$$y2024
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