Subcortical18F-AV-1451 binding patterns in progressive supranuclear palsy.
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.



The objectives of this study were to investigate cortical and subcortical18F-AV-1451 binding patterns in patients with PSP.



We recruited 14 PSP patients and compared their cortical and subcortical binding patterns in18F-AV-1451 positron emission tomography (PET) studies with those of 15 Parkinson's disease (PD) patients and 15 healthy controls.



In both the PD and PSP groups, subcortical18F-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 greater18F-AV-1451 binding in the putamen, globus pallidus, subthalamic nucleus, and dentate nucleus when compared with the controls, whereas the PD patients showed lower18F-AV-1451 binding in the substantia nigra than controls.



The PSP and PD patients showed distinct subcortical18F-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, the18F-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 of18F-AV-1451 PET for PSP patients. © 2016 International Parkinson and Movement Disorder Society.
Department of Neurology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea.
Hanna
H
Cho
Department of Nuclear Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea.
Jae Yong
JY
Choi
Department of Neurology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea.
Mi Song
MS
Hwang
Department of Neurology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea.
Seung Ha
SH
Lee
Department of Nuclear Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea.
Young Hoon
YH
Ryu
Department of Neurology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea.
Myung Sik
MS
Lee
Department of Neurology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea.
Chul Hyoung
CH
Lyoo
D000368:Aged; D002243:Carbolines; D002529:Cerebellar Nuclei / Q000000981:diagnostic imaging / Q000378:metabolism*; D005260:Female; D005917:Globus Pallidus / Q000000981:diagnostic imaging / Q000378:metabolism*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010300:Parkinson Disease / Q000000981:diagnostic imaging / Q000378:metabolism*; D049268:Positron-Emission Tomography / Q000379:methods*; D011699:Putamen / Q000000981:diagnostic imaging / Q000378:metabolism*; D020531:Subthalamic Nucleus / Q000000981:diagnostic imaging / Q000378:metabolism*; D013494:Supranuclear Palsy, Progressive / Q000000981:diagnostic imaging / Q000378:metabolism*; D016875:tau Proteins / Q000378:metabolism*
D002243:Carbolines; D016875:tau Proteins; C000591008:7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole
18F-AV-1451; PET; Parkinson's disease; Progressive supranuclear palsy; tau