Subcortical 18F-AV-1451 binding patterns in progressive supranuclear palsy

Hanna Cho, Jae Yong Choi, Mi Song Hwang, Seung Ha Lee, Young Hoon Ryu, Myung Sik Lee, Chulhyoung Lyoo

Research output: Contribution to journalArticle

51 Citations (Scopus)

Abstract

Background: Accumulation of cortical and subcortical tau pathology is the primary pathological substrate for progressive supranuclear palsy (PSP). 18F-AV-1451, a radiotracer that binds to the pathological tau protein, may be helpful for in vivo visualization and quantitation of tau pathology in PSP. Objectives: The objectives of this study were to investigate cortical and subcortical 18F-AV-1451 binding patterns in patients with PSP. Methods: We recruited 14 PSP patients and compared their cortical and subcortical binding patterns in 18F-AV-1451 positron emission tomography (PET) studies with those of 15 Parkinson's disease (PD) patients and 15 healthy controls. Results: In both the PD and PSP groups, subcortical 18F-AV-1451 binding did not correlate with the severity of motor dysfunctions, and cortical binding did not differ between the controls and each patient group. However, the PSP patients showed greater 18F-AV-1451 binding in the putamen, globus pallidus, subthalamic nucleus, and dentate nucleus when compared with the controls, whereas the PD patients showed lower 18F-AV-1451 binding in the substantia nigra than controls. Conclusions: The PSP and PD patients showed distinct subcortical 18F-AV-1451 binding patterns reflecting subcortical tau pathology in PSP and reduced nigral neuromelanin in PD. However, there was no correlation with the severity of motor dysfunction, no cortical regions with increased binding in PSP patients, and variable degrees of subcortical binding even in the controls. Therefore, the 18F-AV-1451 PET may be less than ideal for assessing tau pathology in PSP. Further studies will be required to validate the clinical correlation and to understand the clinical utility of 18F-AV-1451 PET for PSP patients.

Original languageEnglish
Pages (from-to)134-140
Number of pages7
JournalMovement Disorders
Volume32
Issue number1
DOIs
Publication statusPublished - 2017 Jan 1

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Progressive Supranuclear Palsy
Parkinson Disease
Positron-Emission Tomography
Pathology
Substantia Nigra
Cerebellar Nuclei
tau Proteins
Subthalamic Nucleus
Globus Pallidus
Putamen

All Science Journal Classification (ASJC) codes

  • Neurology
  • Clinical Neurology

Cite this

Cho, H., Choi, J. Y., Hwang, M. S., Lee, S. H., Ryu, Y. H., Lee, M. S., & Lyoo, C. (2017). Subcortical 18F-AV-1451 binding patterns in progressive supranuclear palsy. Movement Disorders, 32(1), 134-140. https://doi.org/10.1002/mds.26844
Cho, Hanna ; Choi, Jae Yong ; Hwang, Mi Song ; Lee, Seung Ha ; Ryu, Young Hoon ; Lee, Myung Sik ; Lyoo, Chulhyoung. / Subcortical 18F-AV-1451 binding patterns in progressive supranuclear palsy. In: Movement Disorders. 2017 ; Vol. 32, No. 1. pp. 134-140.
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abstract = "Background: Accumulation of cortical and subcortical tau pathology is the primary pathological substrate for progressive supranuclear palsy (PSP). 18F-AV-1451, a radiotracer that binds to the pathological tau protein, may be helpful for in vivo visualization and quantitation of tau pathology in PSP. Objectives: The objectives of this study were to investigate cortical and subcortical 18F-AV-1451 binding patterns in patients with PSP. Methods: We recruited 14 PSP patients and compared their cortical and subcortical binding patterns in 18F-AV-1451 positron emission tomography (PET) studies with those of 15 Parkinson's disease (PD) patients and 15 healthy controls. Results: In both the PD and PSP groups, subcortical 18F-AV-1451 binding did not correlate with the severity of motor dysfunctions, and cortical binding did not differ between the controls and each patient group. However, the PSP patients showed greater 18F-AV-1451 binding in the putamen, globus pallidus, subthalamic nucleus, and dentate nucleus when compared with the controls, whereas the PD patients showed lower 18F-AV-1451 binding in the substantia nigra than controls. Conclusions: The PSP and PD patients showed distinct subcortical 18F-AV-1451 binding patterns reflecting subcortical tau pathology in PSP and reduced nigral neuromelanin in PD. However, there was no correlation with the severity of motor dysfunction, no cortical regions with increased binding in PSP patients, and variable degrees of subcortical binding even in the controls. Therefore, the 18F-AV-1451 PET may be less than ideal for assessing tau pathology in PSP. Further studies will be required to validate the clinical correlation and to understand the clinical utility of 18F-AV-1451 PET for PSP patients.",
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Cho, H, Choi, JY, Hwang, MS, Lee, SH, Ryu, YH, Lee, MS & Lyoo, C 2017, 'Subcortical 18F-AV-1451 binding patterns in progressive supranuclear palsy', Movement Disorders, vol. 32, no. 1, pp. 134-140. https://doi.org/10.1002/mds.26844

Subcortical 18F-AV-1451 binding patterns in progressive supranuclear palsy. / Cho, Hanna; Choi, Jae Yong; Hwang, Mi Song; Lee, Seung Ha; Ryu, Young Hoon; Lee, Myung Sik; Lyoo, Chulhyoung.

In: Movement Disorders, Vol. 32, No. 1, 01.01.2017, p. 134-140.

Research output: Contribution to journalArticle

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T1 - Subcortical 18F-AV-1451 binding patterns in progressive supranuclear palsy

AU - Cho, Hanna

AU - Choi, Jae Yong

AU - Hwang, Mi Song

AU - Lee, Seung Ha

AU - Ryu, Young Hoon

AU - Lee, Myung Sik

AU - Lyoo, Chulhyoung

PY - 2017/1/1

Y1 - 2017/1/1

N2 - Background: Accumulation of cortical and subcortical tau pathology is the primary pathological substrate for progressive supranuclear palsy (PSP). 18F-AV-1451, a radiotracer that binds to the pathological tau protein, may be helpful for in vivo visualization and quantitation of tau pathology in PSP. Objectives: The objectives of this study were to investigate cortical and subcortical 18F-AV-1451 binding patterns in patients with PSP. Methods: We recruited 14 PSP patients and compared their cortical and subcortical binding patterns in 18F-AV-1451 positron emission tomography (PET) studies with those of 15 Parkinson's disease (PD) patients and 15 healthy controls. Results: In both the PD and PSP groups, subcortical 18F-AV-1451 binding did not correlate with the severity of motor dysfunctions, and cortical binding did not differ between the controls and each patient group. However, the PSP patients showed greater 18F-AV-1451 binding in the putamen, globus pallidus, subthalamic nucleus, and dentate nucleus when compared with the controls, whereas the PD patients showed lower 18F-AV-1451 binding in the substantia nigra than controls. Conclusions: The PSP and PD patients showed distinct subcortical 18F-AV-1451 binding patterns reflecting subcortical tau pathology in PSP and reduced nigral neuromelanin in PD. However, there was no correlation with the severity of motor dysfunction, no cortical regions with increased binding in PSP patients, and variable degrees of subcortical binding even in the controls. Therefore, the 18F-AV-1451 PET may be less than ideal for assessing tau pathology in PSP. Further studies will be required to validate the clinical correlation and to understand the clinical utility of 18F-AV-1451 PET for PSP patients.

AB - Background: Accumulation of cortical and subcortical tau pathology is the primary pathological substrate for progressive supranuclear palsy (PSP). 18F-AV-1451, a radiotracer that binds to the pathological tau protein, may be helpful for in vivo visualization and quantitation of tau pathology in PSP. Objectives: The objectives of this study were to investigate cortical and subcortical 18F-AV-1451 binding patterns in patients with PSP. Methods: We recruited 14 PSP patients and compared their cortical and subcortical binding patterns in 18F-AV-1451 positron emission tomography (PET) studies with those of 15 Parkinson's disease (PD) patients and 15 healthy controls. Results: In both the PD and PSP groups, subcortical 18F-AV-1451 binding did not correlate with the severity of motor dysfunctions, and cortical binding did not differ between the controls and each patient group. However, the PSP patients showed greater 18F-AV-1451 binding in the putamen, globus pallidus, subthalamic nucleus, and dentate nucleus when compared with the controls, whereas the PD patients showed lower 18F-AV-1451 binding in the substantia nigra than controls. Conclusions: The PSP and PD patients showed distinct subcortical 18F-AV-1451 binding patterns reflecting subcortical tau pathology in PSP and reduced nigral neuromelanin in PD. However, there was no correlation with the severity of motor dysfunction, no cortical regions with increased binding in PSP patients, and variable degrees of subcortical binding even in the controls. Therefore, the 18F-AV-1451 PET may be less than ideal for assessing tau pathology in PSP. Further studies will be required to validate the clinical correlation and to understand the clinical utility of 18F-AV-1451 PET for PSP patients.

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Cho H, Choi JY, Hwang MS, Lee SH, Ryu YH, Lee MS et al. Subcortical 18F-AV-1451 binding patterns in progressive supranuclear palsy. Movement Disorders. 2017 Jan 1;32(1):134-140. https://doi.org/10.1002/mds.26844