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000139503 0247_ $$2doi$$a10.1016/j.neuroimage.2017.05.058
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000139503 0247_ $$2ISSN$$a1053-8119
000139503 0247_ $$2ISSN$$a1095-9572
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000139503 037__ $$aDZNE-2020-05825
000139503 041__ $$aEnglish
000139503 082__ $$a610
000139503 1001_ $$0P:(DE-2719)2811815$$aMaaß, Anne$$b0$$eFirst author$$udzne
000139503 245__ $$aComparison of multiple tau-PET measures as biomarkers in aging and Alzheimer's disease.
000139503 260__ $$aOrlando, Fla.$$bAcademic Press$$c2017
000139503 264_1 $$2Crossref$$3print$$bElsevier BV$$c2017-08-01
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000139503 520__ $$aThe recent development of tau-specific positron emission tomography (PET) tracers enables in vivo quantification of regional tau pathology, one of the key lesions in Alzheimer's disease (AD). Tau PET imaging may become a useful biomarker for clinical diagnosis and tracking of disease progression but there is no consensus yet on how tau PET signal is best quantified. The goal of the current study was to evaluate multiple whole-brain and region-specific approaches to detect clinically relevant tau PET signal. Two independent cohorts of cognitively normal adults and amyloid-positive (Aβ+) patients with mild cognitive impairment (MCI) or AD-dementia underwent [18F]AV-1451 PET. Methods for tau tracer quantification included: (i) in vivo Braak staging, (ii) regional uptake in Braak composite regions, (iii) several whole-brain measures of tracer uptake, (iv) regional uptake in AD-vulnerable voxels, and (v) uptake in a priori defined regions. Receiver operating curves characterized accuracy in distinguishing Aβ- controls from AD/MCI patients and yielded tau positivity cutoffs. Clinical relevance of tau PET measures was assessed by regressions against cognition and MR imaging measures. Key tracer uptake patterns were identified by a factor analysis and voxel-wise contrasts. Braak staging, global and region-specific tau measures yielded similar diagnostic accuracies, which differed between cohorts. While all tau measures were related to amyloid and global cognition, memory and hippocampal/entorhinal volume/thickness were associated with regional tracer retention in the medial temporal lobe. Key regions of tau accumulation included medial temporal and inferior/middle temporal regions, retrosplenial cortex, and banks of the superior temporal sulcus. Our data indicate that whole-brain tau PET measures might be adequate biomarkers to detect AD-related tau pathology. However, regional measures covering AD-vulnerable regions may increase sensitivity to early tau PET signal, atrophy and memory decline.
000139503 536__ $$0G:(DE-HGF)POF3-344$$a344 - Clinical and Health Care Research (POF3-344)$$cPOF3-344$$fPOF III$$x0
000139503 542__ $$2Crossref$$i2017-08-01$$uhttps://www.elsevier.com/tdm/userlicense/1.0/
000139503 542__ $$2Crossref$$i2018-06-21$$uhttp://www.elsevier.com/open-access/userlicense/1.0/
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000139503 650_7 $$2NLM Chemicals$$aAmyloid beta-Peptides
000139503 650_7 $$2NLM Chemicals$$aCarbolines
000139503 650_7 $$2NLM Chemicals$$atau Proteins
000139503 650_7 $$0J09QS3Z3WB$$2NLM Chemicals$$a7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole
000139503 650_2 $$2MeSH$$aAdult
000139503 650_2 $$2MeSH$$aAge of Onset
000139503 650_2 $$2MeSH$$aAged
000139503 650_2 $$2MeSH$$aAged, 80 and over
000139503 650_2 $$2MeSH$$aAging: metabolism
000139503 650_2 $$2MeSH$$aAlzheimer Disease: diagnostic imaging
000139503 650_2 $$2MeSH$$aAlzheimer Disease: metabolism
000139503 650_2 $$2MeSH$$aAlzheimer Disease: pathology
000139503 650_2 $$2MeSH$$aAlzheimer Disease: physiopathology
000139503 650_2 $$2MeSH$$aAmyloid beta-Peptides: metabolism
000139503 650_2 $$2MeSH$$aCarbolines
000139503 650_2 $$2MeSH$$aCognitive Dysfunction: diagnostic imaging
000139503 650_2 $$2MeSH$$aCognitive Dysfunction: metabolism
000139503 650_2 $$2MeSH$$aCognitive Dysfunction: pathology
000139503 650_2 $$2MeSH$$aCognitive Dysfunction: physiopathology
000139503 650_2 $$2MeSH$$aCohort Studies
000139503 650_2 $$2MeSH$$aFemale
000139503 650_2 $$2MeSH$$aHumans
000139503 650_2 $$2MeSH$$aMale
000139503 650_2 $$2MeSH$$aMiddle Aged
000139503 650_2 $$2MeSH$$aNeocortex: diagnostic imaging
000139503 650_2 $$2MeSH$$aNeocortex: metabolism
000139503 650_2 $$2MeSH$$aPositron-Emission Tomography: methods
000139503 650_2 $$2MeSH$$aSeverity of Illness Index
000139503 650_2 $$2MeSH$$aYoung Adult
000139503 650_2 $$2MeSH$$atau Proteins: metabolism
000139503 7001_ $$aLandau, Susan$$b1
000139503 7001_ $$aBaker, Suzanne L$$b2
000139503 7001_ $$aHorng, Andy$$b3
000139503 7001_ $$aLockhart, Samuel N$$b4
000139503 7001_ $$aLa Joie, Renaud$$b5
000139503 7001_ $$aRabinovici, Gil D$$b6
000139503 7001_ $$aJagust, William J$$b7
000139503 7001_ $$aInitiative, Alzheimer's Disease Neuroimaging$$b8
000139503 77318 $$2Crossref$$3journal-article$$a10.1016/j.neuroimage.2017.05.058$$b : Elsevier BV, 2017-08-01$$p448-463$$tNeuroImage$$v157$$x1053-8119$$y2017
000139503 773__ $$0PERI:(DE-600)1471418-8$$a10.1016/j.neuroimage.2017.05.058$$gVol. 157, p. 448 - 463$$p448-463$$q157<448 - 463$$tNeuroImage$$v157$$x1053-8119$$y2017
000139503 8567_ $$2Pubmed Central$$uhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC5814575
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