Sifting through the surfeit of neuroinflammation tracers

The first phase of molecular brain imaging of microglial activation in neuroinflammatory conditions began some 20 years ago with the introduction of [11C]-(R)-PK11195, the prototype isoquinoline ligand for translocator protein (18 kDa) (TSPO). Investigations by positron emission tomography (PET) rev...

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Published inJournal of cerebral blood flow and metabolism Vol. 38; no. 2; pp. 204 - 224
Main Authors Cumming, Paul, Burgher, Bjorn, Patkar, Omkar, Breakspear, Michael, Vasdev, Neil, Thomas, Paul, Liu, Guo-Jun, Banati, Richard
Format Journal Article
LanguageEnglish
Published London, England SAGE Publications 01.02.2018
Subjects
Biomarkers - analysis
Humans
Inflammation - diagnosis
Inflammation - diagnostic imaging
Inflammation - pathology
Microglia - pathology
Nervous System Diseases - diagnosis
Nervous System Diseases - diagnostic imaging
Nervous System Diseases - metabolism
Positron-Emission Tomography
Review
Tomography, Emission-Computed, Single-Photon
positron emission tomography
neuroinflammation
microglia
Translocator protein
quantitation
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Abstract The first phase of molecular brain imaging of microglial activation in neuroinflammatory conditions began some 20 years ago with the introduction of [11C]-(R)-PK11195, the prototype isoquinoline ligand for translocator protein (18 kDa) (TSPO). Investigations by positron emission tomography (PET) revealed microgliosis in numerous brain diseases, despite the rather low specific binding signal imparted by [11C]-(R)-PK11195. There has since been enormous expansion of the repertoire of TSPO tracers, many with higher specific binding, albeit complicated by allelic dependence of the affinity. However, the specificity of TSPO PET for revealing microglial activation not been fully established, and it has been difficult to judge the relative merits of the competing tracers and analysis methods with respect to their sensitivity for detecting microglial activation. We therefore present a systematic comparison of 13 TSPO PET and single photon computed tomography (SPECT) tracers belonging to five structural classes, each of which has been investigated by compartmental analysis in healthy human brain relative to a metabolite-corrected arterial input. We emphasize the need to establish the non-displaceable binding component for each ligand and conclude with five recommendations for a standard approach to define the cellular distribution of TSPO signals, and to characterize the properties of candidate TSPO tracers.
AbstractList The first phase of molecular brain imaging of microglial activation in neuroinflammatory conditions began some 20 years ago with the introduction of [ C]-( R)-PK11195, the prototype isoquinoline ligand for translocator protein (18 kDa) (TSPO). Investigations by positron emission tomography (PET) revealed microgliosis in numerous brain diseases, despite the rather low specific binding signal imparted by [ C]-( R)-PK11195. There has since been enormous expansion of the repertoire of TSPO tracers, many with higher specific binding, albeit complicated by allelic dependence of the affinity. However, the specificity of TSPO PET for revealing microglial activation not been fully established, and it has been difficult to judge the relative merits of the competing tracers and analysis methods with respect to their sensitivity for detecting microglial activation. We therefore present a systematic comparison of 13 TSPO PET and single photon computed tomography (SPECT) tracers belonging to five structural classes, each of which has been investigated by compartmental analysis in healthy human brain relative to a metabolite-corrected arterial input. We emphasize the need to establish the non-displaceable binding component for each ligand and conclude with five recommendations for a standard approach to define the cellular distribution of TSPO signals, and to characterize the properties of candidate TSPO tracers.
The first phase of molecular brain imaging of microglial activation in neuroinflammatory conditions began some 20 years ago with the introduction of [ 11 C]-( R)-PK11195, the prototype isoquinoline ligand for translocator protein (18 kDa) (TSPO). Investigations by positron emission tomography (PET) revealed microgliosis in numerous brain diseases, despite the rather low specific binding signal imparted by [ 11 C]-( R)-PK11195. There has since been enormous expansion of the repertoire of TSPO tracers, many with higher specific binding, albeit complicated by allelic dependence of the affinity. However, the specificity of TSPO PET for revealing microglial activation not been fully established, and it has been difficult to judge the relative merits of the competing tracers and analysis methods with respect to their sensitivity for detecting microglial activation. We therefore present a systematic comparison of 13 TSPO PET and single photon computed tomography (SPECT) tracers belonging to five structural classes, each of which has been investigated by compartmental analysis in healthy human brain relative to a metabolite-corrected arterial input. We emphasize the need to establish the non-displaceable binding component for each ligand and conclude with five recommendations for a standard approach to define the cellular distribution of TSPO signals, and to characterize the properties of candidate TSPO tracers.
The first phase of molecular brain imaging of microglial activation in neuroinflammatory conditions began some 20 years ago with the introduction of [ 11 C]-( R )-PK11195, the prototype isoquinoline ligand for translocator protein (18 kDa) (TSPO). Investigations by positron emission tomography (PET) revealed microgliosis in numerous brain diseases, despite the rather low specific binding signal imparted by [ 11 C]-( R )-PK11195. There has since been enormous expansion of the repertoire of TSPO tracers, many with higher specific binding, albeit complicated by allelic dependence of the affinity. However, the specificity of TSPO PET for revealing microglial activation not been fully established, and it has been difficult to judge the relative merits of the competing tracers and analysis methods with respect to their sensitivity for detecting microglial activation. We therefore present a systematic comparison of 13 TSPO PET and single photon computed tomography (SPECT) tracers belonging to five structural classes, each of which has been investigated by compartmental analysis in healthy human brain relative to a metabolite-corrected arterial input. We emphasize the need to establish the non-displaceable binding component for each ligand and conclude with five recommendations for a standard approach to define the cellular distribution of TSPO signals, and to characterize the properties of candidate TSPO tracers.
The first phase of molecular brain imaging of microglial activation in neuroinflammatory conditions began some 20 years ago with the introduction of [11C]-( R)-PK11195, the prototype isoquinoline ligand for translocator protein (18 kDa) (TSPO). Investigations by positron emission tomography (PET) revealed microgliosis in numerous brain diseases, despite the rather low specific binding signal imparted by [11C]-( R)-PK11195. There has since been enormous expansion of the repertoire of TSPO tracers, many with higher specific binding, albeit complicated by allelic dependence of the affinity. However, the specificity of TSPO PET for revealing microglial activation not been fully established, and it has been difficult to judge the relative merits of the competing tracers and analysis methods with respect to their sensitivity for detecting microglial activation. We therefore present a systematic comparison of 13 TSPO PET and single photon computed tomography (SPECT) tracers belonging to five structural classes, each of which has been investigated by compartmental analysis in healthy human brain relative to a metabolite-corrected arterial input. We emphasize the need to establish the non-displaceable binding component for each ligand and conclude with five recommendations for a standard approach to define the cellular distribution of TSPO signals, and to characterize the properties of candidate TSPO tracers.The first phase of molecular brain imaging of microglial activation in neuroinflammatory conditions began some 20 years ago with the introduction of [11C]-( R)-PK11195, the prototype isoquinoline ligand for translocator protein (18 kDa) (TSPO). Investigations by positron emission tomography (PET) revealed microgliosis in numerous brain diseases, despite the rather low specific binding signal imparted by [11C]-( R)-PK11195. There has since been enormous expansion of the repertoire of TSPO tracers, many with higher specific binding, albeit complicated by allelic dependence of the affinity. However, the specificity of TSPO PET for revealing microglial activation not been fully established, and it has been difficult to judge the relative merits of the competing tracers and analysis methods with respect to their sensitivity for detecting microglial activation. We therefore present a systematic comparison of 13 TSPO PET and single photon computed tomography (SPECT) tracers belonging to five structural classes, each of which has been investigated by compartmental analysis in healthy human brain relative to a metabolite-corrected arterial input. We emphasize the need to establish the non-displaceable binding component for each ligand and conclude with five recommendations for a standard approach to define the cellular distribution of TSPO signals, and to characterize the properties of candidate TSPO tracers.
The first phase of molecular brain imaging of microglial activation in neuroinflammatory conditions began some 20 years ago with the introduction of [11C]-(R)-PK11195, the prototype isoquinoline ligand for translocator protein (18 kDa) (TSPO). Investigations by positron emission tomography (PET) revealed microgliosis in numerous brain diseases, despite the rather low specific binding signal imparted by [11C]-(R)-PK11195. There has since been enormous expansion of the repertoire of TSPO tracers, many with higher specific binding, albeit complicated by allelic dependence of the affinity. However, the specificity of TSPO PET for revealing microglial activation not been fully established, and it has been difficult to judge the relative merits of the competing tracers and analysis methods with respect to their sensitivity for detecting microglial activation. We therefore present a systematic comparison of 13 TSPO PET and single photon computed tomography (SPECT) tracers belonging to five structural classes, each of which has been investigated by compartmental analysis in healthy human brain relative to a metabolite-corrected arterial input. We emphasize the need to establish the non-displaceable binding component for each ligand and conclude with five recommendations for a standard approach to define the cellular distribution of TSPO signals, and to characterize the properties of candidate TSPO tracers.
Author Patkar, Omkar
Banati, Richard
Vasdev, Neil
Thomas, Paul
Breakspear, Michael
Liu, Guo-Jun
Burgher, Bjorn
Cumming, Paul
AuthorAffiliation 1 School of Psychology and Counselling and IHBI, Faculty of Health, Queensland University of Technology, Brisbane, Australia
3 Metro North Mental Health Service, Brisbane, Australia
4 Division of Nuclear Medicine and Molecular Imaging, Massachusetts General Hospital, Boston, MA, USA
8 National Imaging Facility, Brain and Mind Centre and Faculty of Health Sciences, University of Sydney, Camperdown, Australia
5 Department of Radiology, Harvard Medical School, Boston, MA, USA
2 56362 QIMR Berghofer Institute , Brisbane, Australia
7 5419 Australian Nuclear Science and Technology Organisation , Lucas Heights, Australia
6 Herston Imaging Research Facility, Faculty of Medicine, 303224 University of Queensland Centre for Clinical Research , Herston, Australia
AuthorAffiliation_xml – name: 2 56362 QIMR Berghofer Institute , Brisbane, Australia
– name: 7 5419 Australian Nuclear Science and Technology Organisation , Lucas Heights, Australia
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– name: 4 Division of Nuclear Medicine and Molecular Imaging, Massachusetts General Hospital, Boston, MA, USA
– name: 6 Herston Imaging Research Facility, Faculty of Medicine, 303224 University of Queensland Centre for Clinical Research , Herston, Australia
– name: 8 National Imaging Facility, Brain and Mind Centre and Faculty of Health Sciences, University of Sydney, Camperdown, Australia
– name: 1 School of Psychology and Counselling and IHBI, Faculty of Health, Queensland University of Technology, Brisbane, Australia
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  surname: Cumming
  fullname: Cumming, Paul
  email: paul.cumming@qut.edu.au
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Issue 2
Keywords positron emission tomography
neuroinflammation
microglia
Translocator protein
quantitation
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Snippet The first phase of molecular brain imaging of microglial activation in neuroinflammatory conditions began some 20 years ago with the introduction of...
The first phase of molecular brain imaging of microglial activation in neuroinflammatory conditions began some 20 years ago with the introduction of [ 11 C]-(...
The first phase of molecular brain imaging of microglial activation in neuroinflammatory conditions began some 20 years ago with the introduction of [ C]-(...
The first phase of molecular brain imaging of microglial activation in neuroinflammatory conditions began some 20 years ago with the introduction of [11C]-(...
The first phase of molecular brain imaging of microglial activation in neuroinflammatory conditions began some 20 years ago with the introduction of [ 11 C]-(...
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Index Database
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StartPage 204
SubjectTerms Biomarkers - analysis
Humans
Inflammation - diagnosis
Inflammation - diagnostic imaging
Inflammation - pathology
Microglia - pathology
Nervous System Diseases - diagnosis
Nervous System Diseases - diagnostic imaging
Nervous System Diseases - metabolism
Positron-Emission Tomography
Review
Tomography, Emission-Computed, Single-Photon
Title Sifting through the surfeit of neuroinflammation tracers
URI https://journals.sagepub.com/doi/full/10.1177/0271678X17748786
https://www.ncbi.nlm.nih.gov/pubmed/29256293
https://www.proquest.com/docview/1978732504
https://pubmed.ncbi.nlm.nih.gov/PMC5951023
Volume 38
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