The Effects of Physiological and Methodological Determinants on F-FDG Mouse Brain Imaging Exemplified in a Double Transgenic Alzheimer Model

Introduction: In this study, the influence of physiological determinants on 18F-fluoro- d -glucose ( 18 F-FDG) brain uptake was evaluated in a mouse model of Alzheimer disease. Materials and Methods: TASTPM (Tg) and age-matched C57BL/6 J (WT) mice were fasted for 10 hours, while another group was fa...

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Main Authors: Steven Deleye MSc, Ann-Marie Waldron MSc, Jill C. Richardson PhD, Mark Schmidt PhD, Xavier Langlois PhD, Sigrid Stroobants MD, PhD, Steven Staelens PhD
Format: Article
Language:English
Published: SAGE Publications 2016-02-01
Series:Molecular Imaging
Online Access:https://doi.org/10.1177/1536012115624919
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author Steven Deleye MSc
Ann-Marie Waldron MSc
Jill C. Richardson PhD
Mark Schmidt PhD
Xavier Langlois PhD
Sigrid Stroobants MD, PhD
Steven Staelens PhD
author_facet Steven Deleye MSc
Ann-Marie Waldron MSc
Jill C. Richardson PhD
Mark Schmidt PhD
Xavier Langlois PhD
Sigrid Stroobants MD, PhD
Steven Staelens PhD
author_sort Steven Deleye MSc
collection DOAJ
description Introduction: In this study, the influence of physiological determinants on 18F-fluoro- d -glucose ( 18 F-FDG) brain uptake was evaluated in a mouse model of Alzheimer disease. Materials and Methods: TASTPM (Tg) and age-matched C57BL/6 J (WT) mice were fasted for 10 hours, while another group was fasted for 20 hours to evaluate the effect of fasting duration. The effect of repeatedly scanning was evaluated by scanning Tg and WT mice at days 1, 4, and 7. Brain 18 F-FDG uptake was evaluated in the thalamus being the most indicative region. Finally, the cerebellum was tested as a reference region for the relative standard uptake value (rSUV). Results: When correcting the brain uptake for glucose, the effect of different fasting durations was attenuated and the anticipated hypometabolism in Tg mice was demonstrated. Also, with repeated scanning, the brain uptake values within a group and the hypometabolism of the Tg mice only remained stable over time when glucose correction was applied. Finally, hypometabolism was also observed in the cerebellum, yielding artificially higher rSUV values for Tg mice. Conclusion: Corrections for blood glucose levels have to be applied when semiquantifying 18 F-FDG brain uptake in mouse models for AD. Potential reference regions for normalization should be thoroughly investigated to ensure that they are not pathologically affected also by afferent connections.
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spelling doaj.art-a367047fc0644842a2d1c1a2ee15907f2024-03-02T09:53:05ZengSAGE PublicationsMolecular Imaging1536-01212016-02-011510.1177/153601211562491910.1177_1536012115624919The Effects of Physiological and Methodological Determinants on F-FDG Mouse Brain Imaging Exemplified in a Double Transgenic Alzheimer ModelSteven Deleye MSc0Ann-Marie Waldron MSc1Jill C. Richardson PhD2Mark Schmidt PhD3Xavier Langlois PhD4Sigrid Stroobants MD, PhD5Steven Staelens PhD6 Molecular Imaging Center Antwerp, University of Antwerp, Antwerp, Belgium Molecular Imaging Center Antwerp, University of Antwerp, Antwerp, Belgium R&D China UK Group, GlaxoSmithKline, Stevenage, United Kingdom Neuroscience Department, Janssen Pharmaceutica NV, Beerse, Belgium Neuroscience Department, Janssen Pharmaceutica NV, Beerse, Belgium Nuclear Medicine Department, University Hospital Antwerp, Antwerp, Belgium Molecular Imaging Center Antwerp, University of Antwerp, Antwerp, BelgiumIntroduction: In this study, the influence of physiological determinants on 18F-fluoro- d -glucose ( 18 F-FDG) brain uptake was evaluated in a mouse model of Alzheimer disease. Materials and Methods: TASTPM (Tg) and age-matched C57BL/6 J (WT) mice were fasted for 10 hours, while another group was fasted for 20 hours to evaluate the effect of fasting duration. The effect of repeatedly scanning was evaluated by scanning Tg and WT mice at days 1, 4, and 7. Brain 18 F-FDG uptake was evaluated in the thalamus being the most indicative region. Finally, the cerebellum was tested as a reference region for the relative standard uptake value (rSUV). Results: When correcting the brain uptake for glucose, the effect of different fasting durations was attenuated and the anticipated hypometabolism in Tg mice was demonstrated. Also, with repeated scanning, the brain uptake values within a group and the hypometabolism of the Tg mice only remained stable over time when glucose correction was applied. Finally, hypometabolism was also observed in the cerebellum, yielding artificially higher rSUV values for Tg mice. Conclusion: Corrections for blood glucose levels have to be applied when semiquantifying 18 F-FDG brain uptake in mouse models for AD. Potential reference regions for normalization should be thoroughly investigated to ensure that they are not pathologically affected also by afferent connections.https://doi.org/10.1177/1536012115624919
spellingShingle Steven Deleye MSc
Ann-Marie Waldron MSc
Jill C. Richardson PhD
Mark Schmidt PhD
Xavier Langlois PhD
Sigrid Stroobants MD, PhD
Steven Staelens PhD
The Effects of Physiological and Methodological Determinants on F-FDG Mouse Brain Imaging Exemplified in a Double Transgenic Alzheimer Model
Molecular Imaging
title The Effects of Physiological and Methodological Determinants on F-FDG Mouse Brain Imaging Exemplified in a Double Transgenic Alzheimer Model
title_full The Effects of Physiological and Methodological Determinants on F-FDG Mouse Brain Imaging Exemplified in a Double Transgenic Alzheimer Model
title_fullStr The Effects of Physiological and Methodological Determinants on F-FDG Mouse Brain Imaging Exemplified in a Double Transgenic Alzheimer Model
title_full_unstemmed The Effects of Physiological and Methodological Determinants on F-FDG Mouse Brain Imaging Exemplified in a Double Transgenic Alzheimer Model
title_short The Effects of Physiological and Methodological Determinants on F-FDG Mouse Brain Imaging Exemplified in a Double Transgenic Alzheimer Model
title_sort effects of physiological and methodological determinants on f fdg mouse brain imaging exemplified in a double transgenic alzheimer model
url https://doi.org/10.1177/1536012115624919
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