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Findings of 18F‐PI‐2620 tau PET imaging in patients with Alzheimer’s disease and healthy controls in relation to the plasma P‐tau181 levels in a Japanese sample
Background Alzheimer’s disease (AD) is the most common cause of dementia worldwide. In AD, abnormal tau accumulates within neurons of the brain, facilitated by extracellular β‐amyloid deposition, leading to neurodegeneration, and eventually, cognitive impairment. As this process is thought to be irr...
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Published in: | Neuropsychopharmacology reports 2022-12, Vol.42 (4), p.437-448 |
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creator | Bun, Shogyoku Moriguchi, Sho Tezuka, Toshiki Sato, Yoshiaki Takahata, Keisuke Seki, Morinobu Nakajima, Shinichiro Yamamoto, Yasuharu Sano, Yasunori Suzuki, Natsumi Morimoto, Ayaka Ueda, Ryo Tabuchi, Hajime Ito, Daisuke Mimura, Masaru |
description | Background
Alzheimer’s disease (AD) is the most common cause of dementia worldwide. In AD, abnormal tau accumulates within neurons of the brain, facilitated by extracellular β‐amyloid deposition, leading to neurodegeneration, and eventually, cognitive impairment. As this process is thought to be irreversible, early identification of abnormal tau in the brain is crucial for the development of new therapeutic interventions.
Aims
18F‐PI‐2620 is one of the second‐generation tau PET tracers with presumably less off‐target binding than its predecessors. Although a few clinical studies have recently reported the use of 18F‐PI‐2620 tau PET in patients with AD, its applicability to AD is yet to be thoroughly examined.
Methods
In the present pilot study, we performed 18F‐PI‐2620 tau PET in seven cases of probable AD (AD group) and seven healthy controls (HC group). Standardized uptake value ratios (SUVR) in regions of interest (ROIs) in the medial temporal region and neocortex were compared between the AD and HC groups. Furthermore, correlations between regional SUVR and plasma p‐tau181 as well as cognitive test scores were also analyzed.
Results
The uptake of 18F‐PI‐2620 was distinctly increased in the AD group across all the ROIs. SUVR in all the target ROIs were significantly correlated with plasma p‐tau181 levels, as well as with MMSE and ADAS‐cog scores.
Discussion & Conclusion
Our results add to accumulating evidence suggesting that 18F‐PI‐2620 is a promising tau PET tracer that allows patients with AD to be distinguished from healthy controls, although a study with a larger sample size is warranted.
The present pilot study examined the ability of 18F‐PI‐2620 tau PET tracer to distinguish between healthy control and Alzheimer's disease, as well as correlations with plasma p‐tau181 and cognitive test results. Though the sample size was small, seven for each group, its SUVR in the target brain regions showed distinct differences between them and high correlations with plasma p‐tau181 and cognitive test results. |
doi_str_mv | 10.1002/npr2.12281 |
format | article |
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Alzheimer’s disease (AD) is the most common cause of dementia worldwide. In AD, abnormal tau accumulates within neurons of the brain, facilitated by extracellular β‐amyloid deposition, leading to neurodegeneration, and eventually, cognitive impairment. As this process is thought to be irreversible, early identification of abnormal tau in the brain is crucial for the development of new therapeutic interventions.
Aims
18F‐PI‐2620 is one of the second‐generation tau PET tracers with presumably less off‐target binding than its predecessors. Although a few clinical studies have recently reported the use of 18F‐PI‐2620 tau PET in patients with AD, its applicability to AD is yet to be thoroughly examined.
Methods
In the present pilot study, we performed 18F‐PI‐2620 tau PET in seven cases of probable AD (AD group) and seven healthy controls (HC group). Standardized uptake value ratios (SUVR) in regions of interest (ROIs) in the medial temporal region and neocortex were compared between the AD and HC groups. Furthermore, correlations between regional SUVR and plasma p‐tau181 as well as cognitive test scores were also analyzed.
Results
The uptake of 18F‐PI‐2620 was distinctly increased in the AD group across all the ROIs. SUVR in all the target ROIs were significantly correlated with plasma p‐tau181 levels, as well as with MMSE and ADAS‐cog scores.
Discussion & Conclusion
Our results add to accumulating evidence suggesting that 18F‐PI‐2620 is a promising tau PET tracer that allows patients with AD to be distinguished from healthy controls, although a study with a larger sample size is warranted.
The present pilot study examined the ability of 18F‐PI‐2620 tau PET tracer to distinguish between healthy control and Alzheimer's disease, as well as correlations with plasma p‐tau181 and cognitive test results. Though the sample size was small, seven for each group, its SUVR in the target brain regions showed distinct differences between them and high correlations with plasma p‐tau181 and cognitive test results.</description><identifier>ISSN: 2574-173X</identifier><identifier>EISSN: 2574-173X</identifier><identifier>DOI: 10.1002/npr2.12281</identifier><language>eng</language><publisher>Hoboken: John Wiley & Sons, Inc</publisher><subject>Alzheimer's disease ; Automation ; Brain research ; Clinical trials ; Cognition & reasoning ; Dementia ; Magnetic resonance imaging ; MMSE ; Plasma ; plasma p‐181 ; positron emission tomography ; Proteins ; tau ; tauADAS‐cog</subject><ispartof>Neuropsychopharmacology reports, 2022-12, Vol.42 (4), p.437-448</ispartof><rights>2022 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of The Japanese Society of Neuropsychopharmacology.</rights><rights>2022. This work is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0002-0815-1431</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2756612722/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2756612722?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,11541,25731,27901,27902,36989,44566,46027,46451,74869</link.rule.ids></links><search><creatorcontrib>Bun, Shogyoku</creatorcontrib><creatorcontrib>Moriguchi, Sho</creatorcontrib><creatorcontrib>Tezuka, Toshiki</creatorcontrib><creatorcontrib>Sato, Yoshiaki</creatorcontrib><creatorcontrib>Takahata, Keisuke</creatorcontrib><creatorcontrib>Seki, Morinobu</creatorcontrib><creatorcontrib>Nakajima, Shinichiro</creatorcontrib><creatorcontrib>Yamamoto, Yasuharu</creatorcontrib><creatorcontrib>Sano, Yasunori</creatorcontrib><creatorcontrib>Suzuki, Natsumi</creatorcontrib><creatorcontrib>Morimoto, Ayaka</creatorcontrib><creatorcontrib>Ueda, Ryo</creatorcontrib><creatorcontrib>Tabuchi, Hajime</creatorcontrib><creatorcontrib>Ito, Daisuke</creatorcontrib><creatorcontrib>Mimura, Masaru</creatorcontrib><title>Findings of 18F‐PI‐2620 tau PET imaging in patients with Alzheimer’s disease and healthy controls in relation to the plasma P‐tau181 levels in a Japanese sample</title><title>Neuropsychopharmacology reports</title><description>Background
Alzheimer’s disease (AD) is the most common cause of dementia worldwide. In AD, abnormal tau accumulates within neurons of the brain, facilitated by extracellular β‐amyloid deposition, leading to neurodegeneration, and eventually, cognitive impairment. As this process is thought to be irreversible, early identification of abnormal tau in the brain is crucial for the development of new therapeutic interventions.
Aims
18F‐PI‐2620 is one of the second‐generation tau PET tracers with presumably less off‐target binding than its predecessors. Although a few clinical studies have recently reported the use of 18F‐PI‐2620 tau PET in patients with AD, its applicability to AD is yet to be thoroughly examined.
Methods
In the present pilot study, we performed 18F‐PI‐2620 tau PET in seven cases of probable AD (AD group) and seven healthy controls (HC group). Standardized uptake value ratios (SUVR) in regions of interest (ROIs) in the medial temporal region and neocortex were compared between the AD and HC groups. Furthermore, correlations between regional SUVR and plasma p‐tau181 as well as cognitive test scores were also analyzed.
Results
The uptake of 18F‐PI‐2620 was distinctly increased in the AD group across all the ROIs. SUVR in all the target ROIs were significantly correlated with plasma p‐tau181 levels, as well as with MMSE and ADAS‐cog scores.
Discussion & Conclusion
Our results add to accumulating evidence suggesting that 18F‐PI‐2620 is a promising tau PET tracer that allows patients with AD to be distinguished from healthy controls, although a study with a larger sample size is warranted.
The present pilot study examined the ability of 18F‐PI‐2620 tau PET tracer to distinguish between healthy control and Alzheimer's disease, as well as correlations with plasma p‐tau181 and cognitive test results. Though the sample size was small, seven for each group, its SUVR in the target brain regions showed distinct differences between them and high correlations with plasma p‐tau181 and cognitive test results.</description><subject>Alzheimer's disease</subject><subject>Automation</subject><subject>Brain research</subject><subject>Clinical trials</subject><subject>Cognition & reasoning</subject><subject>Dementia</subject><subject>Magnetic resonance imaging</subject><subject>MMSE</subject><subject>Plasma</subject><subject>plasma p‐181</subject><subject>positron emission tomography</subject><subject>Proteins</subject><subject>tau</subject><subject>tauADAS‐cog</subject><issn>2574-173X</issn><issn>2574-173X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpNkc1uEzEUhUcIJKrSDU9giXWKf2bs8bKqGgiqSoSKxM66k7mTceTYg-1QhVUfgS1v0Ofqk-AkCLGwfWV99xxfn6p6y-glo5S_91Pkl4zzlr2oznij6hlT4tvL_-rX1UVKG1rgwxL1WfU0t763fp1IGAhr58-Pv5aLsnHJKcmwI8ube2K3sC4MsZ5MkC36nMiDzSO5cj9HtFuMz4-_E-ltQkhIwPdkRHB53JNV8DkGlw69EV3pDp7kQPKIZHKQtkCWxa44sZYRhz_wxAL5BBN4LHIJtpPDN9WrAVzCi7_nefV1fnN__XF2-_nD4vrqdtYLqtlMC62HjmPT6mE1ACra665My7CpmZJcsr5TILVuWEs70XCJIFdKK1BIoaPivFqcdPsAGzPFMnvcmwDWHC9CXBuI2a4cGiGF6sovohS65jXopkMNQ6NocaFdV7TenbSmGL7vMGWzCbvoy_MNV42UjCvOC8VO1IN1uP9nyag5pGoOqZpjquZu-YUfK_EHAGyZiw</recordid><startdate>202212</startdate><enddate>202212</enddate><creator>Bun, Shogyoku</creator><creator>Moriguchi, Sho</creator><creator>Tezuka, Toshiki</creator><creator>Sato, Yoshiaki</creator><creator>Takahata, Keisuke</creator><creator>Seki, Morinobu</creator><creator>Nakajima, Shinichiro</creator><creator>Yamamoto, Yasuharu</creator><creator>Sano, Yasunori</creator><creator>Suzuki, Natsumi</creator><creator>Morimoto, Ayaka</creator><creator>Ueda, Ryo</creator><creator>Tabuchi, Hajime</creator><creator>Ito, Daisuke</creator><creator>Mimura, Masaru</creator><general>John Wiley & Sons, Inc</general><general>Wiley</general><scope>24P</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-0815-1431</orcidid></search><sort><creationdate>202212</creationdate><title>Findings of 18F‐PI‐2620 tau PET imaging in patients with Alzheimer’s disease and healthy controls in relation to the plasma P‐tau181 levels in a Japanese sample</title><author>Bun, Shogyoku ; Moriguchi, Sho ; Tezuka, Toshiki ; Sato, Yoshiaki ; Takahata, Keisuke ; Seki, Morinobu ; Nakajima, Shinichiro ; Yamamoto, Yasuharu ; Sano, Yasunori ; Suzuki, Natsumi ; Morimoto, Ayaka ; Ueda, Ryo ; Tabuchi, Hajime ; Ito, Daisuke ; Mimura, Masaru</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-d3091-9399fb2e589fcfae70d9b2001e54176261db7a6995180b3526ea6c797a7e0ab03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Alzheimer's disease</topic><topic>Automation</topic><topic>Brain research</topic><topic>Clinical trials</topic><topic>Cognition & reasoning</topic><topic>Dementia</topic><topic>Magnetic resonance imaging</topic><topic>MMSE</topic><topic>Plasma</topic><topic>plasma p‐181</topic><topic>positron emission tomography</topic><topic>Proteins</topic><topic>tau</topic><topic>tauADAS‐cog</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bun, Shogyoku</creatorcontrib><creatorcontrib>Moriguchi, Sho</creatorcontrib><creatorcontrib>Tezuka, Toshiki</creatorcontrib><creatorcontrib>Sato, Yoshiaki</creatorcontrib><creatorcontrib>Takahata, Keisuke</creatorcontrib><creatorcontrib>Seki, Morinobu</creatorcontrib><creatorcontrib>Nakajima, Shinichiro</creatorcontrib><creatorcontrib>Yamamoto, Yasuharu</creatorcontrib><creatorcontrib>Sano, Yasunori</creatorcontrib><creatorcontrib>Suzuki, Natsumi</creatorcontrib><creatorcontrib>Morimoto, Ayaka</creatorcontrib><creatorcontrib>Ueda, Ryo</creatorcontrib><creatorcontrib>Tabuchi, Hajime</creatorcontrib><creatorcontrib>Ito, Daisuke</creatorcontrib><creatorcontrib>Mimura, Masaru</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Publicly Available Content Database (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>Directory of Open Access Journals</collection><jtitle>Neuropsychopharmacology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bun, Shogyoku</au><au>Moriguchi, Sho</au><au>Tezuka, Toshiki</au><au>Sato, Yoshiaki</au><au>Takahata, Keisuke</au><au>Seki, Morinobu</au><au>Nakajima, Shinichiro</au><au>Yamamoto, Yasuharu</au><au>Sano, Yasunori</au><au>Suzuki, Natsumi</au><au>Morimoto, Ayaka</au><au>Ueda, Ryo</au><au>Tabuchi, Hajime</au><au>Ito, Daisuke</au><au>Mimura, Masaru</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Findings of 18F‐PI‐2620 tau PET imaging in patients with Alzheimer’s disease and healthy controls in relation to the plasma P‐tau181 levels in a Japanese sample</atitle><jtitle>Neuropsychopharmacology reports</jtitle><date>2022-12</date><risdate>2022</risdate><volume>42</volume><issue>4</issue><spage>437</spage><epage>448</epage><pages>437-448</pages><issn>2574-173X</issn><eissn>2574-173X</eissn><abstract>Background
Alzheimer’s disease (AD) is the most common cause of dementia worldwide. In AD, abnormal tau accumulates within neurons of the brain, facilitated by extracellular β‐amyloid deposition, leading to neurodegeneration, and eventually, cognitive impairment. As this process is thought to be irreversible, early identification of abnormal tau in the brain is crucial for the development of new therapeutic interventions.
Aims
18F‐PI‐2620 is one of the second‐generation tau PET tracers with presumably less off‐target binding than its predecessors. Although a few clinical studies have recently reported the use of 18F‐PI‐2620 tau PET in patients with AD, its applicability to AD is yet to be thoroughly examined.
Methods
In the present pilot study, we performed 18F‐PI‐2620 tau PET in seven cases of probable AD (AD group) and seven healthy controls (HC group). Standardized uptake value ratios (SUVR) in regions of interest (ROIs) in the medial temporal region and neocortex were compared between the AD and HC groups. Furthermore, correlations between regional SUVR and plasma p‐tau181 as well as cognitive test scores were also analyzed.
Results
The uptake of 18F‐PI‐2620 was distinctly increased in the AD group across all the ROIs. SUVR in all the target ROIs were significantly correlated with plasma p‐tau181 levels, as well as with MMSE and ADAS‐cog scores.
Discussion & Conclusion
Our results add to accumulating evidence suggesting that 18F‐PI‐2620 is a promising tau PET tracer that allows patients with AD to be distinguished from healthy controls, although a study with a larger sample size is warranted.
The present pilot study examined the ability of 18F‐PI‐2620 tau PET tracer to distinguish between healthy control and Alzheimer's disease, as well as correlations with plasma p‐tau181 and cognitive test results. Though the sample size was small, seven for each group, its SUVR in the target brain regions showed distinct differences between them and high correlations with plasma p‐tau181 and cognitive test results.</abstract><cop>Hoboken</cop><pub>John Wiley & Sons, Inc</pub><doi>10.1002/npr2.12281</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-0815-1431</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Alzheimer's disease Automation Brain research Clinical trials Cognition & reasoning Dementia Magnetic resonance imaging MMSE Plasma plasma p‐181 positron emission tomography Proteins tau tauADAS‐cog |
title | Findings of 18F‐PI‐2620 tau PET imaging in patients with Alzheimer’s disease and healthy controls in relation to the plasma P‐tau181 levels in a Japanese sample |
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