TY - JOUR
T1 - PBB3 imaging in Parkinsonian disorders
T2 - Evidence for binding to tau and other proteins
AU - Perez-Soriano, Alexandra
AU - Arena, Julieta E
AU - Dinelle, Katie
AU - Miao, Qing
AU - McKenzie, Jessamyn
AU - Neilson, Nicole
AU - Puschmann, Andreas
AU - Schaffer, Paul
AU - Shinotoh, Hitoshi
AU - Smith-Forrester, Jenna
AU - Shahinfard, Elham
AU - Vafai, Nasim
AU - Wile, Daryl
AU - Wszolek, Zbigniew K
AU - Higuchi, Makoto
AU - Sossi, Vesna
AU - Stoessl, A. Jon
N1 - © 2017 International Parkinson and Movement Disorder Society.
PY - 2017
Y1 - 2017
N2 - 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.
AB - 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.
U2 - 10.1002/mds.27029
DO - 10.1002/mds.27029
M3 - Article
C2 - 28568506
SN - 0885-3185
VL - 32
SP - 1016
EP - 1024
JO - Movement Disorders
JF - Movement Disorders
IS - 7
ER -