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In vivo tracking of tau pathologies with 18F-PM-PBB3 (18F-APN-1607) PET in AD and diverse non-AD tauopathies

https://repo.qst.go.jp/records/79742
https://repo.qst.go.jp/records/79742
6dbdd039-6f50-4c1e-9a0d-b015f191af96
Item type 会議発表用資料 / Presentation(1)
公開日 2020-04-01
タイトル
タイトル In vivo tracking of tau pathologies with 18F-PM-PBB3 (18F-APN-1607) PET in AD and diverse non-AD tauopathies
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
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 Shimada, Hitoshi

× Shimada, Hitoshi

WEKO 862054

Shimada, Hitoshi

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Kubota, Manabu

× Kubota, Manabu

WEKO 862055

Kubota, Manabu

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Takahata, Keisuke

× Takahata, Keisuke

WEKO 862056

Takahata, Keisuke

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Takado, Yuhei

× Takado, Yuhei

WEKO 862057

Takado, Yuhei

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Seki, Chie

× Seki, Chie

WEKO 862058

Seki, Chie

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Ono, Maiko

× Ono, Maiko

WEKO 862059

Ono, Maiko

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Sahara, Naruhiko

× Sahara, Naruhiko

WEKO 862060

Sahara, Naruhiko

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Kawamura, Kazunori

× Kawamura, Kazunori

WEKO 862061

Kawamura, Kazunori

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Ming-Rong, Zhang

× Ming-Rong, Zhang

WEKO 862062

Ming-Rong, Zhang

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Suhara, Tetsuya

× Suhara, Tetsuya

WEKO 862063

Suhara, Tetsuya

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Higuchi, Makoto

× Higuchi, Makoto

WEKO 862064

Higuchi, Makoto

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Shimada, Hitoshi

× Shimada, Hitoshi

WEKO 862065

en Shimada, Hitoshi

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Kubota, Manabu

× Kubota, Manabu

WEKO 862066

en Kubota, Manabu

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Takahata, Keisuke

× Takahata, Keisuke

WEKO 862067

en Takahata, Keisuke

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Takado, Yuhei

× Takado, Yuhei

WEKO 862068

en Takado, Yuhei

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Seki, Chie

× Seki, Chie

WEKO 862069

en Seki, Chie

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Ono, Maiko

× Ono, Maiko

WEKO 862070

en Ono, Maiko

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Sahara, Naruhiko

× Sahara, Naruhiko

WEKO 862071

en Sahara, Naruhiko

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Kawamura, Kazunori

× Kawamura, Kazunori

WEKO 862072

en Kawamura, Kazunori

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Ming-Rong, Zhang

× Ming-Rong, Zhang

WEKO 862073

en Ming-Rong, Zhang

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Suhara, Tetsuya

× Suhara, Tetsuya

WEKO 862074

en Suhara, Tetsuya

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Higuchi, Makoto

× Higuchi, Makoto

WEKO 862075

en Higuchi, Makoto

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抄録
内容記述タイプ Abstract
内容記述 Background: Our previous studies demonstrated 18F-PM-PBB3 (18F-APN-1607) to be a promising PET ligand, with suitable pharmacokinetics, high contrast and minimal parenchymal off-target binding, for quantifying tau pathologies in Alzheimer’s disease (AD) and non-AD tauopathy patients. The present study aims to investigate the association between distribution pattern of PM-PBB3 and clinical features in patients with 4-repeat tauopathies.
Method: We enrolled 17 patients with 4-repeat tauopathies including clinically diagnosed progressive supranuclear palsy (PSP), corticobasal syndrome (CBS), and one patient with corticobasal degeneration (CBD) confirmed by brain biopsy. Seven AD spectrum patients, two Parkinson’s disease (PD) patients, and 15 cognitively healthy controls (HCs) were also recruited. All participants underwent PET scans with 18F-PM-PBB3 and 11C-PiB for estimating regional tau and amyloid-β (Aβ) loads. We generated parametric images of the standardized uptake value ratio (SUVR) to the cerebellar cortex for PM-PBB3 and PiB to evaluate brain regional tau and amyloid-βAβ loads.
Result: We confirmed that all patients with AD spectrum were PiB-positive, while all other participants were PiB-negative. 18F-PM-PBB3 PET showed a characteristic distribution pattern in patients with 4-repeat tauopathies, which was distinct from that observed in AD spectrum patients. Patients with 4-repeat tauopathies showed remarkable uptake of PM-PBB3 especially around subthalamic nucleus, basal ganglia, midbrain including nigra and red nucleus, and dentate nucleus, whereas PD patients did not show any prominent parenchymal uptake of PM-PBB3. Compared with PSP with Richardson syndrome, patients with other PSP-variants including PSP with progressive gait freezing, predominant parkinsonism, ocular motor dysfunction, and CBS/CBD showed relatively milder uptake of PM-PBB3 especially around the midbrain. In contrast, patients with 4-repeat tauopathies presenting behavioral and/or verbal symptoms also presented increased PM-PBB3 uptake in some cortices in addition to the above-mentioned regions. Interestingly, some cognitively healthy elderly showed elevated PM-PBB3 uptake with slight white matter atrophy, which resembled patients with 4-repeat tauopathies in terms of distribution pattern, despite the fact that they were PiB-negative and cognitively normal.
Conclusion: Our results support the hypothesis that distribution of PM-PBB3 may reflect clinical manifestations of 4-repeat tauopathies. 18F-PM-PBB3 PET may facilitate better understanding of the pathological basis of, and drug development for 4-repeat tau pathologies.
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 The Alzheimer's Imaging Consortium (AIC2019)
発表年月日
日付 2019-07-13
日付タイプ Issued
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