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Findings of <scp><sup>18</sup>F‐PI</scp>‐2620 tau <scp>PET</scp> 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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- Shogyoku Bun
- Department of Neuropsychiatry Keio University School of Medicine Tokyo Japan
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- Sho Moriguchi
- Department of Neuropsychiatry Keio University School of Medicine Tokyo Japan
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- Toshiki Tezuka
- Department of Neurology Keio University School of Medicine Tokyo Japan
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- Yoshiaki Sato
- Eisai‐Keio Innovation Laboratory for Dementia hhcData Creation Center Eisai Co., Ltd. Tokyo Japan
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- Keisuke Takahata
- Department of Neuropsychiatry Keio University School of Medicine Tokyo Japan
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- Morinobu Seki
- Department of Neurology Keio University School of Medicine Tokyo Japan
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- Shinichiro Nakajima
- Department of Neuropsychiatry Keio University School of Medicine Tokyo Japan
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- Yasuharu Yamamoto
- Department of Neuropsychiatry Keio University School of Medicine Tokyo Japan
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- Yasunori Sano
- Department of Neuropsychiatry Keio University School of Medicine Tokyo Japan
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- Natsumi Suzuki
- Department of Neuropsychiatry Keio University School of Medicine Tokyo Japan
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- Ayaka Morimoto
- Department of Neuropsychiatry Keio University School of Medicine Tokyo Japan
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- Ryo Ueda
- Office of Radiation Technology Keio University Hospital Tokyo Japan
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- Hajime Tabuchi
- Department of Neuropsychiatry Keio University School of Medicine Tokyo Japan
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- Daisuke Ito
- Department of Neurology Keio University School of Medicine Tokyo Japan
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- Masaru Mimura
- Department of Neuropsychiatry Keio University School of Medicine Tokyo Japan
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Description
<jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>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.</jats:p></jats:sec><jats:sec><jats:title>Aims</jats:title><jats:p><jats:sup>18</jats:sup>F‐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 <jats:sup>18</jats:sup>F‐PI‐2620 tau PET in patients with AD, its applicability to AD is yet to be thoroughly examined.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>In the present pilot study, we performed <jats:sup>18</jats:sup>F‐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.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>The uptake of <jats:sup>18</jats:sup>F‐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.</jats:p></jats:sec><jats:sec><jats:title>Discussion & Conclusion</jats:title><jats:p>Our results add to accumulating evidence suggesting that <jats:sup>18</jats:sup>F‐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.</jats:p></jats:sec>
Journal
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- Neuropsychopharmacology Reports
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Neuropsychopharmacology Reports 42 (4), 437-448, 2022-07-17
Wiley
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Keywords
Details 詳細情報について
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- CRID
- 1360017280641783168
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- ISSN
- 2574173X
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- Article Type
- journal article
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- Data Source
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- Crossref
- KAKEN
- OpenAIRE