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However, contributions of tau\nand amyloid-β (Aβ) depositions, pathological hallmarks\nof AD, to the manifestation of apathy remain elusive.\nMethods S eventeen patients with AD underwent\npositron emission tomography (PET) with 11C-pyridinylbutadienyl-\nbenzothiazole 3 (11C-PBB3) and\n11C-Pittsburgh compound-B (11C-PiB) to estimate tau\nand Aβ accumulations using standardised uptake value\nratio (SUVR) images. 11C-PBB3 and 11C-PiB SUVR were\ncompared between AD patients with high and low\nApathy Scale (AS) scores. Additionally, volumetric and\ndiffusion tensor MRI was performed in those areas where\nany significant difference was observed in PET analyses.\nCorrelation and path analyses among AS and estimated\nimaging parameters were also conducted.\nResults A D patients with high AS scores showed higher\n11C-PBB3 SUVR in the orbitofrontal cortex (OFC) than\nthose with low AS scores, while 11C-PiB SUVR in any\nbrain regions did not differ between them. Elevated\n11C-PBB3 SUVR in OFC, decreased OFC thickness and\ndecreased fractional anisotropy (FA) in the uncinate\nfasciculus (UNC), which is structurally connected to OFC,\ncorrelated significantly with increased scores of the AS.\nPath analysis indicated that increased 11C-PBB3 SUVR in\nOFC affects apathy directly and through reduction of OFC\nthickness and subsequent decrease of FA in UNC.\nConclusions The present findings suggested that tau\npathology in OFC may provoke focal neurotoxicity in OFC\nand the following disruption of the OFC-UNC network,\nleading to the emergence and progression of apathy in\nAD.", "subitem_description_type": "Abstract"}]}, "item_8_publisher_8": {"attribute_name": "出版者", "attribute_value_mlt": [{"subitem_publisher": "BMJ Journals"}]}, "item_8_relation_13": {"attribute_name": "PubMed番号", "attribute_value_mlt": [{"subitem_relation_type_id": {"subitem_relation_type_id_text": "29884723", "subitem_relation_type_select": "PMID"}}]}, "item_8_relation_14": 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Tau-induced focal neurotoxicity and network disruption related to apathy in Alzheimer's disease
https://repo.qst.go.jp/records/49082
https://repo.qst.go.jp/records/49082315f5f00-af67-4452-a35f-5e4c7f3cf09d
Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2018-06-08 | |||||
タイトル | ||||||
タイトル | Tau-induced focal neurotoxicity and network disruption related to apathy in Alzheimer's disease | |||||
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_6501 | |||||
資源タイプ | journal article | |||||
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 |
Kitamura, Soichiro
× Kitamura, Soichiro× Shimada, Hitoshi× Niwa, Fumitoshi× Endo, Hironobu× Shinoto, Hitoshi× Takahata, Keisuke× Kubota, Manabu× Takado, Yuhei× Hirano, Shigeki× Kimura, Yasuyuki× Ming-Rong, Zhang× Kuwabara, Satoshi× Suhara, Tetsuya× Higuchi, Makoto× Kitamura, Soichiro× Shimada, Hitoshi× Niwa, Fumitoshi× Endo, Hironobu× Shinoto, Hitoshi× Takahata, Keisuke× Kubota, Manabu× Takado, Yuhei× Hirano, Shigeki× Kimura, Yasuyuki× Ming-Rong, Zhang× Suhara, Tetsuya× Higuchi, Makoto |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Objective A pathy is a common neuropsychological symptom in Alzheimer’s disease (AD), and previous studies demonstrated that neuronal loss and network disruption in some brain regions play pivotal roles in the pathogenesis of apathy. However, contributions of tau and amyloid-β (Aβ) depositions, pathological hallmarks of AD, to the manifestation of apathy remain elusive. Methods S eventeen patients with AD underwent positron emission tomography (PET) with 11C-pyridinylbutadienyl- benzothiazole 3 (11C-PBB3) and 11C-Pittsburgh compound-B (11C-PiB) to estimate tau and Aβ accumulations using standardised uptake value ratio (SUVR) images. 11C-PBB3 and 11C-PiB SUVR were compared between AD patients with high and low Apathy Scale (AS) scores. Additionally, volumetric and diffusion tensor MRI was performed in those areas where any significant difference was observed in PET analyses. Correlation and path analyses among AS and estimated imaging parameters were also conducted. Results A D patients with high AS scores showed higher 11C-PBB3 SUVR in the orbitofrontal cortex (OFC) than those with low AS scores, while 11C-PiB SUVR in any brain regions did not differ between them. Elevated 11C-PBB3 SUVR in OFC, decreased OFC thickness and decreased fractional anisotropy (FA) in the uncinate fasciculus (UNC), which is structurally connected to OFC, correlated significantly with increased scores of the AS. Path analysis indicated that increased 11C-PBB3 SUVR in OFC affects apathy directly and through reduction of OFC thickness and subsequent decrease of FA in UNC. Conclusions The present findings suggested that tau pathology in OFC may provoke focal neurotoxicity in OFC and the following disruption of the OFC-UNC network, leading to the emergence and progression of apathy in AD. |
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書誌情報 |
Journal of Neurolory, Neurosurgery & Psychiatry 巻 89, 号 11, p. 1208-1214, 発行日 2018-11 |
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出版者 | ||||||
出版者 | BMJ Journals | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0022-3050 | |||||
PubMed番号 | ||||||
識別子タイプ | PMID | |||||
関連識別子 | 29884723 | |||||
DOI | ||||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1136/jnnp-2018-317970 | |||||
関連サイト | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://jnnp.bmj.com/content/89/11/1208 |