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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container_end_page 140
container_issue 1
container_start_page 134
container_title Movement disorders
container_volume 32
creator Cho, Hanna
Choi, Jae Yong
Hwang, Mi Song
Lee, Seung Ha
Ryu, Young Hoon
Lee, Myung Sik
Lyoo, Chul Hyoung
description 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
doi_str_mv 10.1002/mds.26844
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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</description><identifier>ISSN: 0885-3185</identifier><identifier>EISSN: 1531-8257</identifier><identifier>DOI: 10.1002/mds.26844</identifier><identifier>CODEN: MOVDEA</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc</publisher><subject>18F‐AV‐1451 ; Dentate nucleus ; Globus pallidus ; Movement disorders ; Neurodegenerative diseases ; Paralysis ; Parkinson's disease ; Pathology ; PET ; Positron emission tomography ; Progressive supranuclear palsy ; Putamen ; Quantitation ; Substantia nigra ; Subthalamic nucleus ; tau ; Tau protein</subject><ispartof>Movement disorders, 2017-01, Vol.32 (1), p.134-140</ispartof><rights>2016 International Parkinson and Movement Disorder Society</rights><rights>2017 International Parkinson and Movement Disorder Society</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fmds.26844$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fmds.26844$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27929,27930,45579,45580</link.rule.ids></links><search><creatorcontrib>Cho, Hanna</creatorcontrib><creatorcontrib>Choi, Jae Yong</creatorcontrib><creatorcontrib>Hwang, Mi Song</creatorcontrib><creatorcontrib>Lee, Seung Ha</creatorcontrib><creatorcontrib>Ryu, Young Hoon</creatorcontrib><creatorcontrib>Lee, Myung Sik</creatorcontrib><creatorcontrib>Lyoo, Chul Hyoung</creatorcontrib><title>Subcortical 18F‐AV‐1451 binding patterns in progressive supranuclear palsy</title><title>Movement disorders</title><description>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</description><subject>18F‐AV‐1451</subject><subject>Dentate nucleus</subject><subject>Globus pallidus</subject><subject>Movement disorders</subject><subject>Neurodegenerative diseases</subject><subject>Paralysis</subject><subject>Parkinson's disease</subject><subject>Pathology</subject><subject>PET</subject><subject>Positron emission tomography</subject><subject>Progressive supranuclear palsy</subject><subject>Putamen</subject><subject>Quantitation</subject><subject>Substantia nigra</subject><subject>Subthalamic nucleus</subject><subject>tau</subject><subject>Tau protein</subject><issn>0885-3185</issn><issn>1531-8257</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNp9kE1OwzAQRi0EEqWw4AaRWKf1-C_2sioUkAosCmwtx3ErV2ka7ATUHUfgjJwE07JmM98snmY-PYQuAY8AYzLeVHFEhGTsCA2AU8gl4cUxGmApeU5B8lN0FuMaYwAOYoAeF31pt6Hz1tQZyNn359fkNQ1gHLLSN5VvVllrus6FJma-ydqwXQUXo393WezbYJre1s6EBNVxd45OlindxV8O0cvs5nl6l8-fbu-nk3m-BkFYKsWUNRZDIaCUwlJaKW6wYMQAVliBNZUFA2CEc6wCQ5USpSvIcukMLhwdoqvD3VTnrXex0-ttH5r0UhMgjNNCEPofBVJAQRRVOFHjA_Xha7fTbfAbE3YasP41qpNRvTeqH64X-4X-APJPavk</recordid><startdate>201701</startdate><enddate>201701</enddate><creator>Cho, Hanna</creator><creator>Choi, Jae Yong</creator><creator>Hwang, Mi Song</creator><creator>Lee, Seung Ha</creator><creator>Ryu, Young Hoon</creator><creator>Lee, Myung Sik</creator><creator>Lyoo, Chul Hyoung</creator><general>Wiley Subscription Services, Inc</general><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>201701</creationdate><title>Subcortical 18F‐AV‐1451 binding patterns in progressive supranuclear palsy</title><author>Cho, Hanna ; Choi, Jae Yong ; Hwang, Mi Song ; Lee, Seung Ha ; Ryu, Young Hoon ; Lee, Myung Sik ; Lyoo, Chul Hyoung</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-j1624-8249cac01761b86c33d95a0642a109091cadc1a11a6ee4d1a3996be72ffea07e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>18F‐AV‐1451</topic><topic>Dentate nucleus</topic><topic>Globus pallidus</topic><topic>Movement disorders</topic><topic>Neurodegenerative diseases</topic><topic>Paralysis</topic><topic>Parkinson's disease</topic><topic>Pathology</topic><topic>PET</topic><topic>Positron emission tomography</topic><topic>Progressive supranuclear palsy</topic><topic>Putamen</topic><topic>Quantitation</topic><topic>Substantia nigra</topic><topic>Subthalamic nucleus</topic><topic>tau</topic><topic>Tau protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cho, Hanna</creatorcontrib><creatorcontrib>Choi, Jae Yong</creatorcontrib><creatorcontrib>Hwang, Mi Song</creatorcontrib><creatorcontrib>Lee, Seung Ha</creatorcontrib><creatorcontrib>Ryu, Young Hoon</creatorcontrib><creatorcontrib>Lee, Myung Sik</creatorcontrib><creatorcontrib>Lyoo, Chul Hyoung</creatorcontrib><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Nursing &amp; Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Movement disorders</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cho, Hanna</au><au>Choi, Jae Yong</au><au>Hwang, Mi Song</au><au>Lee, Seung Ha</au><au>Ryu, Young Hoon</au><au>Lee, Myung Sik</au><au>Lyoo, Chul Hyoung</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Subcortical 18F‐AV‐1451 binding patterns in progressive supranuclear palsy</atitle><jtitle>Movement disorders</jtitle><date>2017-01</date><risdate>2017</risdate><volume>32</volume><issue>1</issue><spage>134</spage><epage>140</epage><pages>134-140</pages><issn>0885-3185</issn><eissn>1531-8257</eissn><coden>MOVDEA</coden><abstract>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</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc</pub><doi>10.1002/mds.26844</doi><tpages>7</tpages></addata></record>
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subjects 18F‐AV‐1451
Dentate nucleus
Globus pallidus
Movement disorders
Neurodegenerative diseases
Paralysis
Parkinson's disease
Pathology
PET
Positron emission tomography
Progressive supranuclear palsy
Putamen
Quantitation
Substantia nigra
Subthalamic nucleus
tau
Tau protein
title Subcortical 18F‐AV‐1451 binding patterns in progressive supranuclear palsy
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