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

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...

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Veröffentlicht in:Movement disorders 2017-01, Vol.32 (1), p.134-140
Hauptverfasser: Cho, Hanna, Choi, Jae Yong, Hwang, Mi Song, Lee, Seung Ha, Ryu, Young Hoon, Lee, Myung Sik, Lyoo, Chul Hyoung
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Sprache:eng
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Zusammenfassung: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. © 2016 International Parkinson and Movement Disorder Society
ISSN:0885-3185
1531-8257
DOI:10.1002/mds.26844