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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
Main Authors: 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
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container_issue 4
container_start_page 437
container_title Neuropsychopharmacology reports
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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.
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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 &amp; 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 &amp; Sons, Inc</publisher><subject>Alzheimer's disease ; Automation ; Brain research ; Clinical trials ; Cognition &amp; 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 &amp; 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 &amp; 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. 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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 &amp; 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. 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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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