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dc.contributor.authorGroot, Colin-
dc.contributor.authorDoré, Vincent-
dc.contributor.authorRobertson, Joanne-
dc.contributor.authorBurnham, Samantha C-
dc.contributor.authorSavage, Greg-
dc.contributor.authorOssenkoppele, Rik-
dc.contributor.authorRowe, Christopher C-
dc.contributor.authorVillemagne, Victor L-
dc.identifier.citationNeurobiology of Aging 2021; 97: 41-48en
dc.description.abstractWe examined whether mesial temporal (Me) tau relates to cognitive performance in 47 amyloid-β (Aβ)-negative, cognitively normal older adults (>60 years old). Me-tau was measured using [18F]flortaucipir-positron emission tomography standardized uptake value ratio. The effect of continuous and categorical (stratified at standardized uptake value ratio = 1.2 [21% Me-positive]) Me-tau on cognition (mini-mental state examination, pre-Alzheimer's cognitive composite, a memory composite, and a nonmemory composite score) was examined using general linear models, and associations between Me-tau and [18F]flortaucipir signal in the neocortex were assessed using voxelwise regressions (continuous) and voxelwise contrasts (categorical). In addition, we assessed the effect of age and Aβ burden on Me-tau. Both continuous and categorical Me-tau was associated with worse cognitive performance across all tests and with higher lateral temporal and parietal [18F]flortaucipir signal. Furthermore, we observed a marginal association between Me-tau and age, whereas there was no association with Aβ burden. Our findings indicate that Me-tau in Aβ-negative cognitively normal individuals, which is likely age-related (i.e., primary age-related tauopathy), might not be as benign as commonly thought.en
dc.subjectMesial temporal lobeen
dc.titleMesial temporal tau is related to worse cognitive performance and greater neocortical tau load in amyloid-β-negative cognitively normal individuals.en
dc.typeJournal Articleen
dc.identifier.journaltitleNeurobiology of Agingen
dc.identifier.affiliationAlzheimer Center Amsterdam, Department of Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands.en
dc.identifier.affiliationCentre of Excellence for Alzheimer's Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University, Joondalup, Western Australia, Australiaen
dc.identifier.affiliationMolecular Imaging and Therapyen
dc.identifier.affiliationDepartment of Psychology, Macquarie University, North Ryde, New South Wales, Australiaen
dc.identifier.affiliationThe Florey Institute, The University of Melbourne, Parkville, Victoria, Australiaen
dc.identifier.affiliationCSIRO Health and Biosecurity, Parkville, Victoria, Australiaen
dc.identifier.affiliationAlzheimer Center Amsterdam, Department of Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands; Clinical Memory Research Unit, Lund University, P663+Q9, Lund, Sweden..en
dc.identifier.pubmedid33130455-é, Vincent
item.fulltextNo Fulltext-
item.openairetypeJournal Article-
item.grantfulltextnone- Imaging and Therapy- Imaging and Therapy- Imaging and Therapy-
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