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Tau PET Imaging of Neurocognitive Disorders Using Newly Developed Tau Ligand [11C]PBB3

https://repo.qst.go.jp/records/71396
https://repo.qst.go.jp/records/71396
25d3aed7-206d-497f-800e-6e0bf92bf9f4
Item type 会議発表用資料 / Presentation(1)
公開日 2013-12-22
タイトル
タイトル Tau PET Imaging of Neurocognitive Disorders Using Newly Developed Tau Ligand [11C]PBB3
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_c94f
資源タイプ conference object
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アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
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内容記述タイプ Abstract
内容記述 Methods: Participants were 13 patients with AD, 6 patients with PIB-positive (amyloid positive) mild cognitive impairments (MCI) and 10 age-matched healthy controls (HCs). One patient with corticobasal syndrome (CBS) was also included as a preliminary examination. Their cognitive functions were assessed by Mini-Mental State Examination (MMSE). PET images were acquired by a Siemens ECAT EXACT HR+ scanner. A dose (about 10 mCi) of [11C]PBB3 was intravenously injected and sequential PET scans were performed for 70 min. Standardized uptake value ratio (SUVR) was calculated using the cerebellar cortex as reference region, and SUVR images were visually assessed in each subject. We also performed PET scan with a plaque-binding agent, [11C]PIB (about 10 mCi), for 70 min and three-dimensional T1-weighted MRI. Cerebral plaque depositions were estimated using SUVR images at 50–70 min after [11C]PIB injection. Parahippocampal grey matter volumes were estimated by voxel-based morphometry. Correlation analysis between MMSE score and mean cortical [11C]PBB3 or [11C]PIB bindings estimated by WFU pickatlas was performed among MCI and AD patients.
\nResults: All HCs and a patient with CBS were PIB-negative, and all MCI and AD patients were PIB-positive. SUVR images of [11C]PBB3-PET demonstrated high accumulation of [11C]PBB3 in the medial temporal cortex of all AD patients, in which binding of [11C]PIB was minimal. Distribution of [11C]PBB3 accumulation observed in AD patients extended to the entire limbic system and subsequently to the neocortex as a function of the disease severity. Interestingly, a subset of HCs also showed noticeable accumulation of [11C]PBB3 confined to the medial temporal cortex, and exhibited mild parahippocampal atrophy. Significant correlation was shown between mean cortical [11C]PBB3 binding and MMSE score among MCI and AD patients, whereas there was no significant correlation between [11C]PIB and MMSE score. Furthermore, increased [11C]PBB3 signals were found in a CBS patient negative for [11C]PIB-PET.
\nConclusions: The present study supported the utility of [11C]PBB3-PET for detecting tau deposition in vivo, in light of distinct spatial distributions of [11C]PBB3 and [11C]PIB retentions in AD patients. Furthermore, the spread of [11C]PBB3 binding may reflect the dementia severity, resembling progression of Braak tau stages. Moreover, the present study also provided the first evidence for in vivo detection of tau lesions in plaque-negative tauopathies. Our next stage clinical study with expanded sample size and wider range of MMSE scores including non-AD tauopatheis is currently ongoing. To understanding the significance of tau accumulation in various brain disease like traumatic brain injury, [11C]PBB3 has potential to detect various types of tau accumulation in living human brain.
\nKeywords: Tau, PET, Alzheimer's disease, non-AD tauopathy, [11C]PBB3
\nDisclosures: T. Suhara, Part 1: I have collaboration work with Taisho Pharmaceutical Co., Ltd., Eisai Co., Ltd, Takeda Pharmaceutical Company limited and Mitsubishi Tanabe Pharma Corporation.; H. Shimada, Nothing to Disclose; M. Maruyama, Nothing to Disclose; H. Shinotoh, Nothing to Disclose; B. Ji, Nothing to Disclose; J. Maeda, Nothing to Disclose; H. Takano, Nothing to Disclose; N. Sahara, Nothing to Disclose; M. Zhang, Nothing to Disclose; H. Ito, Nothing to Disclose; M. Higuchi, Nothing to
会議概要(会議名, 開催地, 会期, 主催者等)
内容記述タイプ Other
内容記述 52nd ACNP Annual Meeting
発表年月日
日付 2013-12-09
日付タイプ Issued
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