Tau pathology as determinant of changes in atrophy and cerebral blood flow: a multi-modal longitudinal imaging study.

Autor: Visser D; Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands. d.visser2@amsterdamumc.nl.; Amsterdam Neuroscience, Neurodegeneration, Amsterdam, The Netherlands. d.visser2@amsterdamumc.nl.; Amsterdam Neuroscience, Brain Imaging, Amsterdam, The Netherlands. d.visser2@amsterdamumc.nl., Verfaillie SCJ; Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Neurodegeneration, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Brain Imaging, Amsterdam, The Netherlands.; Medical Psychology, Amsterdam UMC Location University of Amsterdam, Meibergdreef 9, Amsterdam, the Netherlands., Bosch I; Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Brain Imaging, Amsterdam, The Netherlands.; Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.; Wallenberg Centre for Molecular and Translational Medicine, University of Gothenburg, Gothenburg, Sweden., Brouwer I; Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Neurodegeneration, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Brain Imaging, Amsterdam, The Netherlands., Tuncel H; Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Neurodegeneration, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Brain Imaging, Amsterdam, The Netherlands., Coomans EM; Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Neurodegeneration, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Brain Imaging, Amsterdam, The Netherlands., Rikken RM; Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Neurodegeneration, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Brain Imaging, Amsterdam, The Netherlands., Mastenbroek SE; Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Neurodegeneration, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Brain Imaging, Amsterdam, The Netherlands.; Clinical Memory Research Unit, Lund University, Lund, Sweden., Golla SSV; Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Neurodegeneration, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Brain Imaging, Amsterdam, The Netherlands., Barkhof F; Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Neurodegeneration, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Brain Imaging, Amsterdam, The Netherlands.; Institutes of Neurology and Healthcare Engineering, University College London, London, UK., van de Giessen E; Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Neurodegeneration, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Brain Imaging, Amsterdam, The Netherlands., van Berckel BNM; Department of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Neurodegeneration, Amsterdam, The Netherlands.; Amsterdam Neuroscience, Brain Imaging, Amsterdam, The Netherlands., van der Flier WM; Amsterdam Neuroscience, Neurodegeneration, Amsterdam, The Netherlands.; Alzheimer Center Amsterdam, Department of Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC location VUmc, Amsterdam, The Netherlands.; Department of Epidemiology and Data Science, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands., Ossenkoppele R; Amsterdam Neuroscience, Neurodegeneration, Amsterdam, The Netherlands. r.ossenkoppele@amsterdamumc.nl.; Clinical Memory Research Unit, Lund University, Lund, Sweden. r.ossenkoppele@amsterdamumc.nl.; Alzheimer Center Amsterdam, Department of Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC location VUmc, Amsterdam, The Netherlands. r.ossenkoppele@amsterdamumc.nl.
Jazyk: angličtina
Zdroj: European journal of nuclear medicine and molecular imaging [Eur J Nucl Med Mol Imaging] 2023 Jul; Vol. 50 (8), pp. 2409-2419. Date of Electronic Publication: 2023 Mar 28.
DOI: 10.1007/s00259-023-06196-2
Abstrakt: Purpose: Tau pathology is associated with concurrent atrophy and decreased cerebral blood flow (CBF) in Alzheimer's disease (AD), but less is known about their temporal relationships. Our aim was therefore to investigate the association of concurrent and longitudinal tau PET with longitudinal changes in atrophy and relative CBF.
Methods: We included 61 individuals from the Amsterdam Dementia Cohort (mean age 65.1 ± 7.5 years, 44% female, 57% amyloid-β positive [Aβ +], 26 cognitively impaired [CI]) who underwent dynamic [ 18 F]flortaucipir PET and structural MRI at baseline and 25 ± 5 months follow-up. In addition, we included 86 individuals (68 CI) who only underwent baseline dynamic [ 18 F]flortaucipir PET and MRI scans to increase power in our statistical models. We obtained [ 18 F]flortaucipir PET binding potential (BP ND ) and R 1 values reflecting tau load and relative CBF, respectively, and computed cortical thickness from the structural MRI scans using FreeSurfer. We assessed the regional associations between i) baseline and ii) annual change in tau PET BP ND in Braak I, III/IV, and V/VI regions and cortical thickness or R 1 in cortical gray matter regions (spanning the whole brain) over time using linear mixed models with random intercepts adjusted for age, sex, time between baseline and follow-up assessments, and baseline BP ND in case of analyses with annual change as determinant. All analyses were performed in Aβ-  cognitively normal (CN) individuals and Aβ+  (CN and CI) individuals separately.
Results: In Aβ+ individuals, greater baseline Braak III/IV and V/VI tau PET binding was associated with faster cortical thinning in primarily frontotemporal regions. Annual changes in tau PET were not associated with cortical thinning over time in either Aβ+ or Aβ-  individuals. Baseline tau PET was not associated with longitudinal changes in relative CBF, but increases in Braak III/IV tau PET over time were associated with increases in parietal relative CBF over time in Aβ + individuals.
Conclusion: We showed that higher tau load was related to accelerated cortical thinning, but not to decreases in relative CBF. Moreover, tau PET load at baseline was a stronger predictor of cortical thinning than change of tau PET signal.
(© 2023. The Author(s).)
Databáze: MEDLINE
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