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PET imaging of [11C]PBR28 in Parkinson’s disease patients does not indicate increased binding to TSPO despite reduced dopamine transporter binding

Purpose To examine the hypothesis that cerebral binding to the 18 kDa translocator protein (TSPO), a marker of microglia activation, is elevated in Parkinson’s disease (PD), and to assess the relationship between brain TSPO binding and dopaminergic pathology in PD. Methods The radioligand [ 11 C]PBR... Full description

Journal Title: European Journal of Nuclear Medicine and Molecular Imaging 2018, Vol.46 (2), p.367-375
Main Author: Varnäs, Katarina
Other Authors: Cselényi, Zsolt , Jucaite, Aurelija , Halldin, Christer , Svenningsson, Per , Farde, Lars , Varrone, Andrea
Format: Electronic Article Electronic Article
Language: English
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Publisher: Berlin/Heidelberg: Springer Berlin Heidelberg
ID: ISSN: 1619-7070
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title: PET imaging of [11C]PBR28 in Parkinson’s disease patients does not indicate increased binding to TSPO despite reduced dopamine transporter binding
format: Article
creator:
  • Varnäs, Katarina
  • Cselényi, Zsolt
  • Jucaite, Aurelija
  • Halldin, Christer
  • Svenningsson, Per
  • Farde, Lars
  • Varrone, Andrea
subjects:
  • 18 kDa translocator protein
  • Affinity
  • Binders
  • Binding
  • Brain
  • Cardiology
  • Diagnostic systems
  • Dopamine
  • Dopamine receptors
  • Dopamine transporter
  • Fluorine isotopes
  • Gene polymorphism
  • Hypotheses
  • Imaging
  • Iron
  • Medical imaging
  • Medicin och hälsovetenskap
  • Medicine
  • Medicine & Public Health
  • Microglia
  • Movement disorders
  • Neurodegenerative diseases
  • Neuroimaging
  • Nuclear Medicine
  • Oncology
  • Original
  • Original Article
  • Orthopedics
  • Parkinson's disease
  • Parkinsons disease
  • Pathology
  • Patients
  • PET imaging
  • Polymorphism
  • Positron emission
  • Positron emission tomography
  • Proteins
  • Radiology
  • Statistical analysis
  • Thalamus
  • Tomography
  • Transporter
  • Variance analysis
ispartof: European Journal of Nuclear Medicine and Molecular Imaging, 2018, Vol.46 (2), p.367-375
description: Purpose To examine the hypothesis that cerebral binding to the 18 kDa translocator protein (TSPO), a marker of microglia activation, is elevated in Parkinson’s disease (PD), and to assess the relationship between brain TSPO binding and dopaminergic pathology in PD. Methods The radioligand [ 11 C]PBR28 was used for quantitative assessment of brain TSPO in 16 control subjects and 16 PD patients. To analyse the relationship between dopaminergic pathology and brain TSPO binding, PET studies of the dopamine transporter (DAT) were undertaken in PD patients using the DAT radioligand [ 18 F]FE-PE2I. The total distribution volume of [ 11 C]PBR28 was quantified in nigrostriatal regions, limbic cortices and thalamus, and the binding potential of [ 18 F]FE-PE2I was quantified in nigrostriatal regions. Results Based on genotype analysis of the TSPO rs6971 polymorphism, 16 subjects (8 control subjects and 8 PD patients) were identified as high-affinity binders, and the remaining subjects were identified as mixed-affinity binders. A two-way ANOVA showed a strong main effect of TSPO genotype on the cerebral binding of [ 11 C]PBR28, whereas no statistically significant main effect of diagnostic group, or a group by genotype interaction was found for any of the regions analysed. [ 18 F]FE-PE2I PET studies in patients indicated a marked reduction in nigrostriatal binding to DAT. However, no correlations between the binding parameters were found for [ 11 C]PBR28 and [ 18 F]FE-PE2I. Conclusion The findings do not support the hypothesis of elevated cerebral TSPO binding or a relationship between TSPO binding and dopaminergic pathology in PD.
language: eng
source:
identifier: ISSN: 1619-7070
fulltext: no_fulltext
issn:
  • 1619-7070
  • 1619-7089
  • 1619-7089
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titlePET imaging of [11C]PBR28 in Parkinson’s disease patients does not indicate increased binding to TSPO despite reduced dopamine transporter binding
creatorVarnäs, Katarina ; Cselényi, Zsolt ; Jucaite, Aurelija ; Halldin, Christer ; Svenningsson, Per ; Farde, Lars ; Varrone, Andrea
creatorcontribVarnäs, Katarina ; Cselényi, Zsolt ; Jucaite, Aurelija ; Halldin, Christer ; Svenningsson, Per ; Farde, Lars ; Varrone, Andrea
descriptionPurpose To examine the hypothesis that cerebral binding to the 18 kDa translocator protein (TSPO), a marker of microglia activation, is elevated in Parkinson’s disease (PD), and to assess the relationship between brain TSPO binding and dopaminergic pathology in PD. Methods The radioligand [ 11 C]PBR28 was used for quantitative assessment of brain TSPO in 16 control subjects and 16 PD patients. To analyse the relationship between dopaminergic pathology and brain TSPO binding, PET studies of the dopamine transporter (DAT) were undertaken in PD patients using the DAT radioligand [ 18 F]FE-PE2I. The total distribution volume of [ 11 C]PBR28 was quantified in nigrostriatal regions, limbic cortices and thalamus, and the binding potential of [ 18 F]FE-PE2I was quantified in nigrostriatal regions. Results Based on genotype analysis of the TSPO rs6971 polymorphism, 16 subjects (8 control subjects and 8 PD patients) were identified as high-affinity binders, and the remaining subjects were identified as mixed-affinity binders. A two-way ANOVA showed a strong main effect of TSPO genotype on the cerebral binding of [ 11 C]PBR28, whereas no statistically significant main effect of diagnostic group, or a group by genotype interaction was found for any of the regions analysed. [ 18 F]FE-PE2I PET studies in patients indicated a marked reduction in nigrostriatal binding to DAT. However, no correlations between the binding parameters were found for [ 11 C]PBR28 and [ 18 F]FE-PE2I. Conclusion The findings do not support the hypothesis of elevated cerebral TSPO binding or a relationship between TSPO binding and dopaminergic pathology in PD.
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subject18 kDa translocator protein ; Affinity ; Binders ; Binding ; Brain ; Cardiology ; Diagnostic systems ; Dopamine ; Dopamine receptors ; Dopamine transporter ; Fluorine isotopes ; Gene polymorphism ; Hypotheses ; Imaging ; Iron ; Medical imaging ; Medicin och hälsovetenskap ; Medicine ; Medicine & Public Health ; Microglia ; Movement disorders ; Neurodegenerative diseases ; Neuroimaging ; Nuclear Medicine ; Oncology ; Original ; Original Article ; Orthopedics ; Parkinson's disease ; Parkinsons disease ; Pathology ; Patients ; PET imaging ; Polymorphism ; Positron emission ; Positron emission tomography ; Proteins ; Radiology ; Statistical analysis ; Thalamus ; Tomography ; Transporter ; Variance analysis
ispartofEuropean Journal of Nuclear Medicine and Molecular Imaging, 2018, Vol.46 (2), p.367-375
rights
0The Author(s) 2018
1European Journal of Nuclear Medicine and Molecular Imaging is a copyright of Springer, (2018). All Rights Reserved. © 2018. 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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1Cselényi, Zsolt
2Jucaite, Aurelija
3Halldin, Christer
4Svenningsson, Per
5Farde, Lars
6Varrone, Andrea
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0PET imaging of [11C]PBR28 in Parkinson’s disease patients does not indicate increased binding to TSPO despite reduced dopamine transporter binding
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descriptionPurpose To examine the hypothesis that cerebral binding to the 18 kDa translocator protein (TSPO), a marker of microglia activation, is elevated in Parkinson’s disease (PD), and to assess the relationship between brain TSPO binding and dopaminergic pathology in PD. Methods The radioligand [ 11 C]PBR28 was used for quantitative assessment of brain TSPO in 16 control subjects and 16 PD patients. To analyse the relationship between dopaminergic pathology and brain TSPO binding, PET studies of the dopamine transporter (DAT) were undertaken in PD patients using the DAT radioligand [ 18 F]FE-PE2I. The total distribution volume of [ 11 C]PBR28 was quantified in nigrostriatal regions, limbic cortices and thalamus, and the binding potential of [ 18 F]FE-PE2I was quantified in nigrostriatal regions. Results Based on genotype analysis of the TSPO rs6971 polymorphism, 16 subjects (8 control subjects and 8 PD patients) were identified as high-affinity binders, and the remaining subjects were identified as mixed-affinity binders. A two-way ANOVA showed a strong main effect of TSPO genotype on the cerebral binding of [ 11 C]PBR28, whereas no statistically significant main effect of diagnostic group, or a group by genotype interaction was found for any of the regions analysed. [ 18 F]FE-PE2I PET studies in patients indicated a marked reduction in nigrostriatal binding to DAT. However, no correlations between the binding parameters were found for [ 11 C]PBR28 and [ 18 F]FE-PE2I. Conclusion The findings do not support the hypothesis of elevated cerebral TSPO binding or a relationship between TSPO binding and dopaminergic pathology in PD.
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13Imaging
14Iron
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36Proteins
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titlePET imaging of [11C]PBR28 in Parkinson’s disease patients does not indicate increased binding to TSPO despite reduced dopamine transporter binding
authorVarnäs, Katarina ; Cselényi, Zsolt ; Jucaite, Aurelija ; Halldin, Christer ; Svenningsson, Per ; Farde, Lars ; Varrone, Andrea
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018 kDa translocator protein
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10Fluorine isotopes
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13Imaging
14Iron
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32PET imaging
33Polymorphism
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36Proteins
37Radiology
38Statistical analysis
39Thalamus
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41Transporter
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0Varnäs, Katarina
1Cselényi, Zsolt
2Jucaite, Aurelija
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atitlePET imaging of [11C]PBR28 in Parkinson’s disease patients does not indicate increased binding to TSPO despite reduced dopamine transporter binding
jtitleEuropean Journal of Nuclear Medicine and Molecular Imaging
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abstractPurpose To examine the hypothesis that cerebral binding to the 18 kDa translocator protein (TSPO), a marker of microglia activation, is elevated in Parkinson’s disease (PD), and to assess the relationship between brain TSPO binding and dopaminergic pathology in PD. Methods The radioligand [ 11 C]PBR28 was used for quantitative assessment of brain TSPO in 16 control subjects and 16 PD patients. To analyse the relationship between dopaminergic pathology and brain TSPO binding, PET studies of the dopamine transporter (DAT) were undertaken in PD patients using the DAT radioligand [ 18 F]FE-PE2I. The total distribution volume of [ 11 C]PBR28 was quantified in nigrostriatal regions, limbic cortices and thalamus, and the binding potential of [ 18 F]FE-PE2I was quantified in nigrostriatal regions. Results Based on genotype analysis of the TSPO rs6971 polymorphism, 16 subjects (8 control subjects and 8 PD patients) were identified as high-affinity binders, and the remaining subjects were identified as mixed-affinity binders. A two-way ANOVA showed a strong main effect of TSPO genotype on the cerebral binding of [ 11 C]PBR28, whereas no statistically significant main effect of diagnostic group, or a group by genotype interaction was found for any of the regions analysed. [ 18 F]FE-PE2I PET studies in patients indicated a marked reduction in nigrostriatal binding to DAT. However, no correlations between the binding parameters were found for [ 11 C]PBR28 and [ 18 F]FE-PE2I. Conclusion The findings do not support the hypothesis of elevated cerebral TSPO binding or a relationship between TSPO binding and dopaminergic pathology in PD.
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