PBB3 imaging in Parkinsonian disorders: Evidence for binding to tau and other proteins

ABSTRACT Background and Objectives: To study selective regional binding for tau pathology in vivo, using PET with [11C]PBB3 in PSP patients, and other conditions not typically associated with tauopathy. Methods: Dynamic PET scans were obtained for 70 minutes after the bolus injection of [11C]PBB3 in...

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Published inMovement disorders Vol. 32; no. 7; pp. 1016 - 1024
Main Authors Perez‐Soriano, Alexandra, Arena, Julieta E., Dinelle, Katie, Miao, Qing, McKenzie, Jessamyn, Neilson, Nicole, Puschmann, Andreas, Schaffer, Paul, Shinotoh, Hitoshi, Smith‐Forrester, Jenna, Shahinfard, Elham, Vafai, Nasim, Wile, Daryl, Wszolek, Zbigniew, Higuchi, Makoto, Sossi, Vesna, Stoessl, A. Jon
Format Journal Article
LanguageEnglish
Published United States Wiley Subscription Services, Inc 01.07.2017
Subjects
Aged
alpha-Synuclein - genetics
alpha-Synuclein - metabolism
Basal ganglia
Basal Ganglia - diagnostic imaging
Basal Ganglia - metabolism
Benzothiazoles
Brain diseases
Carbon Radioisotopes
Central nervous system diseases
Cerebellum
Clinical Medicine
Dynactin Complex - genetics
Frontal lobe
Humans
Image processing
Klinisk medicin
Medical and Health Sciences
Medicin och hälsovetenskap
Mesencephalon
Middle Aged
Movement disorders
MSA
Multiple System Atrophy - diagnostic imaging
Multiple System Atrophy - metabolism
Neostriatum
Neurodegenerative diseases
Neurologi
Neurology
Nuclei
Parietal lobe
Parkinsonian Disorders - diagnostic imaging
Parkinsonian Disorders - metabolism
PBB3
Pedunculopontine tegmental nucleus
Positron-Emission Tomography - methods
PSP
Putamen
SNCA mutations
Substantia alba
Supranuclear Palsy, Progressive - diagnostic imaging
Supranuclear Palsy, Progressive - metabolism
Synuclein
Tau PET imaging
Tau protein
tau Proteins - metabolism
Temporal lobe
Thalamus
SNCA mutations
MSA
PSP
Tau PET imaging
PBB3
Online AccessGet full text
ISSN0885-3185
1531-8257
1531-8257
DOI10.1002/mds.27029

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Abstract ABSTRACT Background and Objectives: To study selective regional binding for tau pathology in vivo, using PET with [11C]PBB3 in PSP patients, and other conditions not typically associated with tauopathy. Methods: Dynamic PET scans were obtained for 70 minutes after the bolus injection of [11C]PBB3 in 5 PSP subjects, 1 subject with DCTN1 mutation and PSP phenotype, 3 asymptomatic SNCA duplication carriers, 1 MSA subject, and 6 healthy controls of similar age. Tissue reference Logan analysis was applied to each region of interest using a cerebellar white matter reference region. Results: In comparison to the control group, PSP subjects showed specific uptake of [11C]PBB3 in putamen, midbrain, GP, and SN. Longer disease duration and more advanced clinical severity were generally associated with higher tracer retention. A DCTN1/PSP phenotype case showed increased binding in putamen, parietal lobe, and GP. In SNCA duplication carriers, there was a significant increase of [11C] PBB3 binding in GP, putamen, thalamus, ventral striatum, SN, and pedunculopontine nucleus. The MSA case showed increased binding in frontal lobe, GP, midbrain, parietal lobe, putamen, temporal lobe, SN, thalamus, and ventral striatum. Conclusions: All PSP patients showed increased retention of the tracer in the basal ganglia, as expected. Binding was also present in asymptomatic SNCA duplication carriers and in an MSA case, which are not typically associated with pathological tau deposition. This suggests the possibility that [11C]PBB3 binds to alpha‐synuclein. © 2017 International Parkinson and Movement Disorder Society
AbstractList Background and Objectives: To study selective regional binding for tau pathology in vivo, using PET with [11C]PBB3 in PSP patients, and other conditions not typically associated with tauopathy. Methods: Dynamic PET scans were obtained for 70 minutes after the bolus injection of [11C]PBB3 in 5 PSP subjects, 1 subject with DCTN1 mutation and PSP phenotype, 3 asymptomatic SNCA duplication carriers, 1 MSA subject, and 6 healthy controls of similar age. Tissue reference Logan analysis was applied to each region of interest using a cerebellar white matter reference region. Results: In comparison to the control group, PSP subjects showed specific uptake of [11C]PBB3 in putamen, midbrain, GP, and SN. Longer disease duration and more advanced clinical severity were generally associated with higher tracer retention. A DCTN1/PSP phenotype case showed increased binding in putamen, parietal lobe, and GP. In SNCA duplication carriers, there was a significant increase of [11C] PBB3 binding in GP, putamen, thalamus, ventral striatum, SN, and pedunculopontine nucleus. The MSA case showed increased binding in frontal lobe, GP, midbrain, parietal lobe, putamen, temporal lobe, SN, thalamus, and ventral striatum. Conclusions: All PSP patients showed increased retention of the tracer in the basal ganglia, as expected. Binding was also present in asymptomatic SNCA duplication carriers and in an MSA case, which are not typically associated with pathological tau deposition. This suggests the possibility that [11C]PBB3 binds to alpha-synuclein. © 2017 International Parkinson and Movement Disorder Society
BACKGROUND AND OBJECTIVES: To study selective regional binding for tau pathology in vivo, using PET with [(11) C]PBB3 in PSP patients, and other conditions not typically associated with tauopathy. METHODS: Dynamic PET scans were obtained for 70 minutes after the bolus injection of [(11) C]PBB3 in 5 PSP subjects, 1 subject with DCTN1 mutation and PSP phenotype, 3 asymptomatic SNCA duplication carriers, 1 MSA subject, and 6 healthy controls of similar age. Tissue reference Logan analysis was applied to each region of interest using a cerebellar white matter reference region. RESULTS: In comparison to the control group, PSP subjects showed specific uptake of [(11) C]PBB3 in putamen, midbrain, GP, and SN. Longer disease duration and more advanced clinical severity were generally associated with higher tracer retention. A DCTN1/PSP phenotype case showed increased binding in putamen, parietal lobe, and GP. In SNCA duplication carriers, there was a significant increase of [(11) C] PBB3 binding in GP, putamen, thalamus, ventral striatum, SN, and pedunculopontine nucleus. The MSA case showed increased binding in frontal lobe, GP, midbrain, parietal lobe, putamen, temporal lobe, SN, thalamus, and ventral striatum. CONCLUSIONS: All PSP patients showed increased retention of the tracer in the basal ganglia, as expected. Binding was also present in asymptomatic SNCA duplication carriers and in an MSA case, which are not typically associated with pathological tau deposition. This suggests the possibility that [(11) C]PBB3 binds to alpha-synuclein. © 2017 International Parkinson and Movement Disorder Society.
ABSTRACT Background and Objectives: To study selective regional binding for tau pathology in vivo, using PET with [11C]PBB3 in PSP patients, and other conditions not typically associated with tauopathy. Methods: Dynamic PET scans were obtained for 70 minutes after the bolus injection of [11C]PBB3 in 5 PSP subjects, 1 subject with DCTN1 mutation and PSP phenotype, 3 asymptomatic SNCA duplication carriers, 1 MSA subject, and 6 healthy controls of similar age. Tissue reference Logan analysis was applied to each region of interest using a cerebellar white matter reference region. Results: In comparison to the control group, PSP subjects showed specific uptake of [11C]PBB3 in putamen, midbrain, GP, and SN. Longer disease duration and more advanced clinical severity were generally associated with higher tracer retention. A DCTN1/PSP phenotype case showed increased binding in putamen, parietal lobe, and GP. In SNCA duplication carriers, there was a significant increase of [11C] PBB3 binding in GP, putamen, thalamus, ventral striatum, SN, and pedunculopontine nucleus. The MSA case showed increased binding in frontal lobe, GP, midbrain, parietal lobe, putamen, temporal lobe, SN, thalamus, and ventral striatum. Conclusions: All PSP patients showed increased retention of the tracer in the basal ganglia, as expected. Binding was also present in asymptomatic SNCA duplication carriers and in an MSA case, which are not typically associated with pathological tau deposition. This suggests the possibility that [11C]PBB3 binds to alpha‐synuclein. © 2017 International Parkinson and Movement Disorder Society
Background and Objectives : To study selective regional binding for tau pathology in vivo, using PET with [ 11 C]PBB3 in PSP patients, and other conditions not typically associated with tauopathy. Methods : Dynamic PET scans were obtained for 70 minutes after the bolus injection of [ 11 C]PBB3 in 5 PSP subjects, 1 subject with DCTN1 mutation and PSP phenotype, 3 asymptomatic SNCA duplication carriers, 1 MSA subject, and 6 healthy controls of similar age. Tissue reference Logan analysis was applied to each region of interest using a cerebellar white matter reference region. Results : In comparison to the control group, PSP subjects showed specific uptake of [ 11 C]PBB3 in putamen, midbrain, GP, and SN. Longer disease duration and more advanced clinical severity were generally associated with higher tracer retention. A DCTN1 /PSP phenotype case showed increased binding in putamen, parietal lobe, and GP. In SNCA duplication carriers, there was a significant increase of [ 11 C] PBB3 binding in GP, putamen, thalamus, ventral striatum, SN, and pedunculopontine nucleus. The MSA case showed increased binding in frontal lobe, GP, midbrain, parietal lobe, putamen, temporal lobe, SN, thalamus, and ventral striatum. Conclusions : All PSP patients showed increased retention of the tracer in the basal ganglia, as expected. Binding was also present in asymptomatic SNCA duplication carriers and in an MSA case, which are not typically associated with pathological tau deposition. This suggests the possibility that [ 11 C]PBB3 binds to alpha‐synuclein. © 2017 International Parkinson and Movement Disorder Society
To study selective regional binding for tau pathology in vivo, using PET with [ C]PBB3 in PSP patients, and other conditions not typically associated with tauopathy. Dynamic PET scans were obtained for 70 minutes after the bolus injection of [ C]PBB3 in 5 PSP subjects, 1 subject with DCTN1 mutation and PSP phenotype, 3 asymptomatic SNCA duplication carriers, 1 MSA subject, and 6 healthy controls of similar age. Tissue reference Logan analysis was applied to each region of interest using a cerebellar white matter reference region. In comparison to the control group, PSP subjects showed specific uptake of [ C]PBB3 in putamen, midbrain, GP, and SN. Longer disease duration and more advanced clinical severity were generally associated with higher tracer retention. A DCTN1/PSP phenotype case showed increased binding in putamen, parietal lobe, and GP. In SNCA duplication carriers, there was a significant increase of [ C] PBB3 binding in GP, putamen, thalamus, ventral striatum, SN, and pedunculopontine nucleus. The MSA case showed increased binding in frontal lobe, GP, midbrain, parietal lobe, putamen, temporal lobe, SN, thalamus, and ventral striatum. All PSP patients showed increased retention of the tracer in the basal ganglia, as expected. Binding was also present in asymptomatic SNCA duplication carriers and in an MSA case, which are not typically associated with pathological tau deposition. This suggests the possibility that [ C]PBB3 binds to alpha-synuclein. © 2017 International Parkinson and Movement Disorder Society.
To study selective regional binding for tau pathology in vivo, using PET with [11 C]PBB3 in PSP patients, and other conditions not typically associated with tauopathy.BACKGROUND AND OBJECTIVESTo study selective regional binding for tau pathology in vivo, using PET with [11 C]PBB3 in PSP patients, and other conditions not typically associated with tauopathy.Dynamic PET scans were obtained for 70 minutes after the bolus injection of [11 C]PBB3 in 5 PSP subjects, 1 subject with DCTN1 mutation and PSP phenotype, 3 asymptomatic SNCA duplication carriers, 1 MSA subject, and 6 healthy controls of similar age. Tissue reference Logan analysis was applied to each region of interest using a cerebellar white matter reference region.METHODSDynamic PET scans were obtained for 70 minutes after the bolus injection of [11 C]PBB3 in 5 PSP subjects, 1 subject with DCTN1 mutation and PSP phenotype, 3 asymptomatic SNCA duplication carriers, 1 MSA subject, and 6 healthy controls of similar age. Tissue reference Logan analysis was applied to each region of interest using a cerebellar white matter reference region.In comparison to the control group, PSP subjects showed specific uptake of [11 C]PBB3 in putamen, midbrain, GP, and SN. Longer disease duration and more advanced clinical severity were generally associated with higher tracer retention. A DCTN1/PSP phenotype case showed increased binding in putamen, parietal lobe, and GP. In SNCA duplication carriers, there was a significant increase of [11 C] PBB3 binding in GP, putamen, thalamus, ventral striatum, SN, and pedunculopontine nucleus. The MSA case showed increased binding in frontal lobe, GP, midbrain, parietal lobe, putamen, temporal lobe, SN, thalamus, and ventral striatum.RESULTSIn comparison to the control group, PSP subjects showed specific uptake of [11 C]PBB3 in putamen, midbrain, GP, and SN. Longer disease duration and more advanced clinical severity were generally associated with higher tracer retention. A DCTN1/PSP phenotype case showed increased binding in putamen, parietal lobe, and GP. In SNCA duplication carriers, there was a significant increase of [11 C] PBB3 binding in GP, putamen, thalamus, ventral striatum, SN, and pedunculopontine nucleus. The MSA case showed increased binding in frontal lobe, GP, midbrain, parietal lobe, putamen, temporal lobe, SN, thalamus, and ventral striatum.All PSP patients showed increased retention of the tracer in the basal ganglia, as expected. Binding was also present in asymptomatic SNCA duplication carriers and in an MSA case, which are not typically associated with pathological tau deposition. This suggests the possibility that [11 C]PBB3 binds to alpha-synuclein. © 2017 International Parkinson and Movement Disorder Society.CONCLUSIONSAll PSP patients showed increased retention of the tracer in the basal ganglia, as expected. Binding was also present in asymptomatic SNCA duplication carriers and in an MSA case, which are not typically associated with pathological tau deposition. This suggests the possibility that [11 C]PBB3 binds to alpha-synuclein. © 2017 International Parkinson and Movement Disorder Society.
Author Stoessl, A. Jon
Miao, Qing
Sossi, Vesna
McKenzie, Jessamyn
Vafai, Nasim
Puschmann, Andreas
Higuchi, Makoto
Wile, Daryl
Smith‐Forrester, Jenna
Perez‐Soriano, Alexandra
Arena, Julieta E.
Shinotoh, Hitoshi
Shahinfard, Elham
Dinelle, Katie
Schaffer, Paul
Neilson, Nicole
Wszolek, Zbigniew
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  organization: National Institute of Radiological Sciences
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  organization: University of British Columbia
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  organization: University of British Columbia
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  fullname: Vafai, Nasim
  organization: University of British Columbia
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  organization: National Institute of Radiological Sciences
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ContentType Journal Article
Copyright 2017 International Parkinson and Movement Disorder Society
2017 International Parkinson and Movement Disorder Society.
Copyright_xml – notice: 2017 International Parkinson and Movement Disorder Society
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MultiPark: Multidisciplinary research focused on Parkinson's disease
Lunds universitet
Profile areas and other strong research environments
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Department of Clinical Sciences, Lund
Neurology, Lund
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IsPeerReviewed true
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Issue 7
Keywords SNCA mutations
MSA
PSP
Tau PET imaging
PBB3
Language English
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2017 International Parkinson and Movement Disorder Society.
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Notes Weston Brain Institute, Canada Research Chairs (AJS), and Pacific Parkinsons Research Institute.
Full financial disclosures and author roles may be found in the online version of this article.
Nothing to report.
Relevant conflicts of interest/financial disclosures
Funding agencies
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Snippet ABSTRACT Background and Objectives: To study selective regional binding for tau pathology in vivo, using PET with [11C]PBB3 in PSP patients, and other...
Background and Objectives : To study selective regional binding for tau pathology in vivo, using PET with [ 11 C]PBB3 in PSP patients, and other conditions not...
To study selective regional binding for tau pathology in vivo, using PET with [ C]PBB3 in PSP patients, and other conditions not typically associated with...
Background and Objectives: To study selective regional binding for tau pathology in vivo, using PET with [11C]PBB3 in PSP patients, and other conditions not...
To study selective regional binding for tau pathology in vivo, using PET with [11 C]PBB3 in PSP patients, and other conditions not typically associated with...
BACKGROUND AND OBJECTIVES: To study selective regional binding for tau pathology in vivo, using PET with [(11) C]PBB3 in PSP patients, and other conditions not...
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SubjectTerms Aged
alpha-Synuclein - genetics
alpha-Synuclein - metabolism
Basal ganglia
Basal Ganglia - diagnostic imaging
Basal Ganglia - metabolism
Benzothiazoles
Brain diseases
Carbon Radioisotopes
Central nervous system diseases
Cerebellum
Clinical Medicine
Dynactin Complex - genetics
Frontal lobe
Humans
Image processing
Klinisk medicin
Medical and Health Sciences
Medicin och hälsovetenskap
Mesencephalon
Middle Aged
Movement disorders
MSA
Multiple System Atrophy - diagnostic imaging
Multiple System Atrophy - metabolism
Neostriatum
Neurodegenerative diseases
Neurologi
Neurology
Nuclei
Parietal lobe
Parkinsonian Disorders - diagnostic imaging
Parkinsonian Disorders - metabolism
PBB3
Pedunculopontine tegmental nucleus
Positron-Emission Tomography - methods
PSP
Putamen
SNCA mutations
Substantia alba
Supranuclear Palsy, Progressive - diagnostic imaging
Supranuclear Palsy, Progressive - metabolism
Synuclein
Tau PET imaging
Tau protein
tau Proteins - metabolism
Temporal lobe
Thalamus
Title PBB3 imaging in Parkinsonian disorders: Evidence for binding to tau and other proteins
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