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

Perez-Soriano, Alexandra; Arena, Julieta E; Dinelle, Katie; Miao, Qing; McKenzie, Jessamyn; Neilson, Nicole; Puschmann, Andreas LU ; Schaffer, Paul; Shinotoh, Hitoshi and Smith-Forrester, Jenna, et al. (2017) In Movement Disorders 32(7). p.1016-1024
Abstract

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... (More)

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.

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type
Contribution to journal
publication status
published
subject
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Movement Disorders
volume
32
issue
7
pages
1016 - 1024
publisher
John Wiley & Sons
external identifiers
  • scopus:85020123983
  • wos:000405488300010
ISSN
0885-3185
DOI
10.1002/mds.27029
language
English
LU publication?
yes
id
144d5967-d1ac-4b12-902a-3f47ad0e4d1e
date added to LUP
2017-07-04 14:41:43
date last changed
2018-03-18 05:14:22
@article{144d5967-d1ac-4b12-902a-3f47ad0e4d1e,
  abstract     = {<p>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.</p><p>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.</p><p>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.</p><p>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.</p>},
  author       = {Perez-Soriano, Alexandra and Arena, Julieta E and Dinelle, Katie and Miao, Qing and McKenzie, Jessamyn and Neilson, Nicole and Puschmann, Andreas and Schaffer, Paul and Shinotoh, Hitoshi and Smith-Forrester, Jenna and Shahinfard, Elham and Vafai, Nasim and Wile, Daryl and Wszolek, Zbigniew K and Higuchi, Makoto and Sossi, Vesna and Stoessl, A. Jon},
  issn         = {0885-3185},
  language     = {eng},
  month        = {06},
  number       = {7},
  pages        = {1016--1024},
  publisher    = {John Wiley & Sons},
  series       = {Movement Disorders},
  title        = {PBB3 imaging in Parkinsonian disorders : Evidence for binding to tau and other proteins},
  url          = {http://dx.doi.org/10.1002/mds.27029},
  volume       = {32},
  year         = {2017},
}