Longitudinal tau and metabolic PET imaging in relation to novel CSF tau measures in Alzheimer’s disease

Purpose Studies comparing CSF and PET tau biomarkers have included only commercial CSF assays examining specific phosphorylation sites (e.g. threonine 181, P-tau 181p ) and mid-domain tau (i.e. total tau, T-tau). Moreover, these studies did not examine CSF tau levels in relation to cerebral glucose...

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Published inEuropean journal of nuclear medicine and molecular imaging Vol. 46; no. 5; pp. 1152 - 1163
Main Authors Leuzy, Antoine, Cicognola, Claudia, Chiotis, Konstantinos, Saint-Aubert, Laure, Lemoine, Laetitia, Andreasen, Niels, Zetterberg, Henrik, Ye, Keqiang, Blennow, Kaj, Höglund, Kina, Nordberg, Agneta
Format Journal Article
LanguageEnglish
Published Berlin/Heidelberg Springer Berlin Heidelberg 01.05.2019
Springer Nature B.V
Springer Verlag (Germany) [1976-....]
Subjects
[F-18]FDG
[F-18]THK5317
Aged
Alzheimer Disease - cerebrospinal fluid
Alzheimer Disease - diagnostic imaging
Alzheimer Disease - metabolism
Alzheimer's disease
Assaying
association
Biomarkers
Cardiology
Cerebrospinal fluid
CSF
Dementia
Dementia disorders
deposition
Female
fluid amyloid-beta
Fluorine isotopes
Fluorodeoxyglucose F18
Glucose
Glucose metabolism
human brain
Humans
Hypometabolism
Imaging
Life Sciences
Longitudinal Studies
Male
Medicine
Medicine & Public Health
Metabolism
Middle Aged
N-Terminus
Neurodegeneration
neurofibrillary pathology
Nuclear Medicine
Nuclear Medicine & Medical Imaging
Oncology
Original
Original Article
Orthopedics
PET imaging
phospho-tau
Phosphorylation
Positron emission
Positron emission tomography
Radiologi och bildbehandling
Radiology
Radiology and Medical Imaging
Tau
Tau protein
tau Proteins - cerebrospinal fluid
Threonine
Tomography
F]THK5317
Alzheimer’s disease
PET imaging
CSF
F]FDG
Tau
[
[18F]THK5317
[18F]FDG
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Abstract Purpose Studies comparing CSF and PET tau biomarkers have included only commercial CSF assays examining specific phosphorylation sites (e.g. threonine 181, P-tau 181p ) and mid-domain tau (i.e. total tau, T-tau). Moreover, these studies did not examine CSF tau levels in relation to cerebral glucose metabolism. We thus aimed to examine CSF tau measures, using both commercial and novel assays, in relation to [ 18 F]THK5317 (tau) and [ 18 F]FDG PET (glucose metabolism). Methods Fourteen Alzheimer’s disease (AD) patients (seven prodromal, seven dementia) underwent [ 18 F]THK5317 and [ 18 F]FDG PET studies, with follow-up performed in ten subjects (six prodromal, four dementia) after 17 months. In addition to commercial assays, novel measures capturing N-terminus+mid-domain (tau N-Mid) and C-terminally truncated (tau-368) fragments were included. Results While the levels of all forms of CSF tau were found to be inversely associated with baseline [ 18 F]FDG uptake, associations with baseline [ 18 F]THK5317 uptake varied in relation to the degree of isocortical hypometabolism ([ 18 F]FDG SUVR). Changes in the levels of the novel CSF markers tracked longitudinal changes in tracer uptake better than changes in P-tau 181p and T-tau levels, and improved concordance with dichotomized regional [ 18 F]THK5317 measures. Conclusion Our findings suggest that neurodegeneration may modulate the relationship between CSF and PET tau biomarkers, and that, by comparison to P-tau 181p and T-tau, tau-368 and tau N-Mid may better capture tau pathology and synaptic impairment.
AbstractList Purpose: Studies comparing CSF and PET tau biomarkers have included only commercial CSF assays examining specific phosphorylation sites (e.g. threonine 181, P-tau181p) and mid-domain tau (i.e. total tau, T-tau). Moreover, these studies did not examine CSF tau levels in relation to cerebral glucose metabolism. We thus aimed to examine CSF tau measures, using both commercial and novel assays, in relation to [18F]THK5317 (tau) and [18F]FDG PET (glucose metabolism).Methods: Fourteen Alzheimer's disease (AD) patients (seven prodromal, seven dementia) underwent [18F]THK5317 and [18F]FDG PET studies, with follow-up performed in ten subjects (six prodromal, four dementia) after 17 months. In addition to commercial assays, novel measures capturing N-terminus+mid-domain (tau N-Mid) and C-terminally truncated (tau-368) fragments were included.Results: While the levels of all forms of CSF tau were found to be inversely associated with baseline [18F]FDG uptake, associations with baseline [18F]THK5317 uptake varied in relation to the degree of isocortical hypometabolism ([18F]FDG SUVR). Changes in the levels of the novel CSF markers tracked longitudinal changes in tracer uptake better than changes in P-tau181p and T-tau levels, and improved concordance with dichotomized regional [18F]THK5317 measures.Conclusion: Our findings suggest that neurodegeneration may modulate the relationship between CSF and PET tau biomarkers, and that, by comparison to P-tau181p and T-tau, tau-368 and tau N-Mid may better capture tau pathology and synaptic impairment.
Purpose Studies comparing CSF and PET tau biomarkers have included only commercial CSF assays examining specific phosphorylation sites (e.g. threonine 181, P-tau 181p ) and mid-domain tau (i.e. total tau, T-tau). Moreover, these studies did not examine CSF tau levels in relation to cerebral glucose metabolism. We thus aimed to examine CSF tau measures, using both commercial and novel assays, in relation to [ 18 F]THK5317 (tau) and [ 18 F]FDG PET (glucose metabolism). Methods Fourteen Alzheimer’s disease (AD) patients (seven prodromal, seven dementia) underwent [ 18 F]THK5317 and [ 18 F]FDG PET studies, with follow-up performed in ten subjects (six prodromal, four dementia) after 17 months. In addition to commercial assays, novel measures capturing N-terminus+mid-domain (tau N-Mid) and C-terminally truncated (tau-368) fragments were included. Results While the levels of all forms of CSF tau were found to be inversely associated with baseline [ 18 F]FDG uptake, associations with baseline [ 18 F]THK5317 uptake varied in relation to the degree of isocortical hypometabolism ([ 18 F]FDG SUVR). Changes in the levels of the novel CSF markers tracked longitudinal changes in tracer uptake better than changes in P-tau 181p and T-tau levels, and improved concordance with dichotomized regional [ 18 F]THK5317 measures. Conclusion Our findings suggest that neurodegeneration may modulate the relationship between CSF and PET tau biomarkers, and that, by comparison to P-tau 181p and T-tau, tau-368 and tau N-Mid may better capture tau pathology and synaptic impairment.
Purpose Studies comparing CSF and PET tau biomarkers have included only commercial CSF assays examining specific phosphorylation sites (e.g. threonine 181, P-tau(181p)) and mid-domain tau (i.e. total tau, T-tau). Moreover, these studies did not examine CSF tau levels in relation to cerebral glucose metabolism. We thus aimed to examine CSF tau measures, using both commercial and novel assays, in relation to [F-18]THK5317 (tau) and [F-18]FDG PET (glucose metabolism). Methods Fourteen Alzheimer's disease (AD) patients (seven prodromal, seven dementia) underwent [F-18]THK5317 and [F-18]FDG PET studies, with follow-up performed in ten subjects (six prodromal, four dementia) after 17 months. In addition to commercial assays, novel measures capturing N-terminus+mid-domain (tau N-Mid) and C-terminally truncated (tau-368) fragments were included. Results While the levels of all forms of CSF tau were found to be inversely associated with baseline [F-18]FDG uptake, associations with baseline [F-18]THK5317 uptake varied in relation to the degree of isocortical hypometabolism ([F-18]FDG SUVR). Changes in the levels of the novel CSF markers tracked longitudinal changes in tracer uptake better than changes in P-tau(181p) and T-tau levels, and improved concordance with dichotomized regional [F-18]THK5317 measures. Conclusion Our findings suggest that neurodegeneration may modulate the relationship between CSF and PET tau biomarkers, and that, by comparison to P-tau(181p) and T-tau, tau-368 and tau N-Mid may better capturetau pathology and synaptic impairment.
Studies comparing CSF and PET tau biomarkers have included only commercial CSF assays examining specific phosphorylation sites (e.g. threonine 181, P-tau ) and mid-domain tau (i.e. total tau, T-tau). Moreover, these studies did not examine CSF tau levels in relation to cerebral glucose metabolism. We thus aimed to examine CSF tau measures, using both commercial and novel assays, in relation to [ F]THK5317 (tau) and [ F]FDG PET (glucose metabolism). Fourteen Alzheimer's disease (AD) patients (seven prodromal, seven dementia) underwent [ F]THK5317 and [ F]FDG PET studies, with follow-up performed in ten subjects (six prodromal, four dementia) after 17 months. In addition to commercial assays, novel measures capturing N-terminus+mid-domain (tau N-Mid) and C-terminally truncated (tau-368) fragments were included. While the levels of all forms of CSF tau were found to be inversely associated with baseline [ F]FDG uptake, associations with baseline [ F]THK5317 uptake varied in relation to the degree of isocortical hypometabolism ([ F]FDG SUVR). Changes in the levels of the novel CSF markers tracked longitudinal changes in tracer uptake better than changes in P-tau and T-tau levels, and improved concordance with dichotomized regional [ F]THK5317 measures. Our findings suggest that neurodegeneration may modulate the relationship between CSF and PET tau biomarkers, and that, by comparison to P-tau and T-tau, tau-368 and tau N-Mid may better capture tau pathology and synaptic impairment.
PurposeStudies comparing CSF and PET tau biomarkers have included only commercial CSF assays examining specific phosphorylation sites (e.g. threonine 181, P-tau181p) and mid-domain tau (i.e. total tau, T-tau). Moreover, these studies did not examine CSF tau levels in relation to cerebral glucose metabolism. We thus aimed to examine CSF tau measures, using both commercial and novel assays, in relation to [18F]THK5317 (tau) and [18F]FDG PET (glucose metabolism).MethodsFourteen Alzheimer’s disease (AD) patients (seven prodromal, seven dementia) underwent [18F]THK5317 and [18F]FDG PET studies, with follow-up performed in ten subjects (six prodromal, four dementia) after 17 months. In addition to commercial assays, novel measures capturing N-terminus+mid-domain (tau N-Mid) and C-terminally truncated (tau-368) fragments were included.ResultsWhile the levels of all forms of CSF tau were found to be inversely associated with baseline [18F]FDG uptake, associations with baseline [18F]THK5317 uptake varied in relation to the degree of isocortical hypometabolism ([18F]FDG SUVR). Changes in the levels of the novel CSF markers tracked longitudinal changes in tracer uptake better than changes in P-tau181p and T-tau levels, and improved concordance with dichotomized regional [18F]THK5317 measures.ConclusionOur findings suggest that neurodegeneration may modulate the relationship between CSF and PET tau biomarkers, and that, by comparison to P-tau181p and T-tau, tau-368 and tau N-Mid may better capture tau pathology and synaptic impairment.
Studies comparing CSF and PET tau biomarkers have included only commercial CSF assays examining specific phosphorylation sites (e.g. threonine 181, P-tau181p) and mid-domain tau (i.e. total tau, T-tau). Moreover, these studies did not examine CSF tau levels in relation to cerebral glucose metabolism. We thus aimed to examine CSF tau measures, using both commercial and novel assays, in relation to [18F]THK5317 (tau) and [18F]FDG PET (glucose metabolism).PURPOSEStudies comparing CSF and PET tau biomarkers have included only commercial CSF assays examining specific phosphorylation sites (e.g. threonine 181, P-tau181p) and mid-domain tau (i.e. total tau, T-tau). Moreover, these studies did not examine CSF tau levels in relation to cerebral glucose metabolism. We thus aimed to examine CSF tau measures, using both commercial and novel assays, in relation to [18F]THK5317 (tau) and [18F]FDG PET (glucose metabolism).Fourteen Alzheimer's disease (AD) patients (seven prodromal, seven dementia) underwent [18F]THK5317 and [18F]FDG PET studies, with follow-up performed in ten subjects (six prodromal, four dementia) after 17 months. In addition to commercial assays, novel measures capturing N-terminus+mid-domain (tau N-Mid) and C-terminally truncated (tau-368) fragments were included.METHODSFourteen Alzheimer's disease (AD) patients (seven prodromal, seven dementia) underwent [18F]THK5317 and [18F]FDG PET studies, with follow-up performed in ten subjects (six prodromal, four dementia) after 17 months. In addition to commercial assays, novel measures capturing N-terminus+mid-domain (tau N-Mid) and C-terminally truncated (tau-368) fragments were included.While the levels of all forms of CSF tau were found to be inversely associated with baseline [18F]FDG uptake, associations with baseline [18F]THK5317 uptake varied in relation to the degree of isocortical hypometabolism ([18F]FDG SUVR). Changes in the levels of the novel CSF markers tracked longitudinal changes in tracer uptake better than changes in P-tau181p and T-tau levels, and improved concordance with dichotomized regional [18F]THK5317 measures.RESULTSWhile the levels of all forms of CSF tau were found to be inversely associated with baseline [18F]FDG uptake, associations with baseline [18F]THK5317 uptake varied in relation to the degree of isocortical hypometabolism ([18F]FDG SUVR). Changes in the levels of the novel CSF markers tracked longitudinal changes in tracer uptake better than changes in P-tau181p and T-tau levels, and improved concordance with dichotomized regional [18F]THK5317 measures.Our findings suggest that neurodegeneration may modulate the relationship between CSF and PET tau biomarkers, and that, by comparison to P-tau181p and T-tau, tau-368 and tau N-Mid may better capture tau pathology and synaptic impairment.CONCLUSIONOur findings suggest that neurodegeneration may modulate the relationship between CSF and PET tau biomarkers, and that, by comparison to P-tau181p and T-tau, tau-368 and tau N-Mid may better capture tau pathology and synaptic impairment.
Author Ye, Keqiang
Saint-Aubert, Laure
Zetterberg, Henrik
Blennow, Kaj
Cicognola, Claudia
Chiotis, Konstantinos
Andreasen, Niels
Höglund, Kina
Nordberg, Agneta
Leuzy, Antoine
Lemoine, Laetitia
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  surname: Saint-Aubert
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  organization: Department of Neurobiology, Care Sciences and Society, Division of Clinical Geriatrics, Karolinska Institutet, Theme Aging, Karolinska University Hospital
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European Journal of Nuclear Medicine and Molecular Imaging is a copyright of Springer, (2019). All Rights Reserved. © 2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
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Issue 5
Keywords F]THK5317
Alzheimer’s disease
PET imaging
CSF
F]FDG
Tau
[
[18F]THK5317
[18F]FDG
Language English
License Attribution: http://creativecommons.org/licenses/by
Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
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PublicationTitle European journal of nuclear medicine and molecular imaging
PublicationTitleAbbrev Eur J Nucl Med Mol Imaging
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Snippet Purpose Studies comparing CSF and PET tau biomarkers have included only commercial CSF assays examining specific phosphorylation sites (e.g. threonine 181,...
Studies comparing CSF and PET tau biomarkers have included only commercial CSF assays examining specific phosphorylation sites (e.g. threonine 181, P-tau ) and...
PurposeStudies comparing CSF and PET tau biomarkers have included only commercial CSF assays examining specific phosphorylation sites (e.g. threonine 181,...
Studies comparing CSF and PET tau biomarkers have included only commercial CSF assays examining specific phosphorylation sites (e.g. threonine 181, P-tau181p)...
Purpose: Studies comparing CSF and PET tau biomarkers have included only commercial CSF assays examining specific phosphorylation sites (e.g. threonine 181,...
Purpose Studies comparing CSF and PET tau biomarkers have included only commercial CSF assays examining specific phosphorylation sites (e.g. threonine 181,...
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SubjectTerms [F-18]FDG
[F-18]THK5317
Aged
Alzheimer Disease - cerebrospinal fluid
Alzheimer Disease - diagnostic imaging
Alzheimer Disease - metabolism
Alzheimer's disease
Assaying
association
Biomarkers
Cardiology
Cerebrospinal fluid
CSF
Dementia
Dementia disorders
deposition
Female
fluid amyloid-beta
Fluorine isotopes
Fluorodeoxyglucose F18
Glucose
Glucose metabolism
human brain
Humans
Hypometabolism
Imaging
Life Sciences
Longitudinal Studies
Male
Medicine
Medicine & Public Health
Metabolism
Middle Aged
N-Terminus
Neurodegeneration
neurofibrillary pathology
Nuclear Medicine
Nuclear Medicine & Medical Imaging
Oncology
Original
Original Article
Orthopedics
PET imaging
phospho-tau
Phosphorylation
Positron emission
Positron emission tomography
Radiologi och bildbehandling
Radiology
Radiology and Medical Imaging
Tau
Tau protein
tau Proteins - cerebrospinal fluid
Threonine
Tomography
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Title Longitudinal tau and metabolic PET imaging in relation to novel CSF tau measures in Alzheimer’s disease
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Volume 46
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