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Loss of Lysosomal Proteins Progranulin and Prosaposin Associated with Increased Neurofibrillary Tangle Development in Alzheimer Disease.
http://hdl.handle.net/10422/00013111
http://hdl.handle.net/10422/0001311162cbe23e-4a5d-47ce-a443-102a85de4951
Item type | 学術雑誌論文 / Journal Article(1) | |||||
---|---|---|---|---|---|---|
公開日 | 2021-11-04 | |||||
タイトル | ||||||
タイトル | Loss of Lysosomal Proteins Progranulin and Prosaposin Associated with Increased Neurofibrillary Tangle Development in Alzheimer Disease. | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Alzheimer disease | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Neuropathology | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Progranulin | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Prosaposin | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Tangles | |||||
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 |
MENDSAIKHAN, Anarmaa
× MENDSAIKHAN, Anarmaa× TOOYAMA, Ikuo× SERRANO, Geidy E× BEACH, Thomas G× WALKER, Douglas Gordon |
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著者別名 |
遠山, 育夫
× 遠山, 育夫 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Alzheimer disease (AD) is a progressive neurodegenerative disease causing cognitive decline in the aging population. To develop disease-modifying treatments, understanding the mechanisms behind the pathology is important, which should include observations using human brain samples. We reported previously on the association of lysosomal proteins progranulin (PGRN) and prosaposin (PSAP) with amyloid plaques in non-demented aged control and AD brains. In this study, we investigated the possible involvement of PGRN and PSAP in tangle formation using human brain tissue sections of non-demented aged control subjects and AD cases and compared with cases of frontotemporal dementia with granulin (GRN) mutations. The study revealed that decreased amounts of PGRN and PSAP proteins were detected even in immature neurofibrillary tangles, while colocalization was still evident in adjacent neurons in all cases. Results suggest that neuronal loss of PGRN preceded loss of PSAP as tangles developed and matured. The GRN mutation cases exhibited almost complete absence of PGRN in most neurons, while PSAP signal was preserved. Although based on correlative data, we suggest that reduced levels of PGRN and PSAP and their interaction in neurons might predispose to accumulation of p-Tau protein. | |||||
書誌情報 |
en : Journal of Neuropathology and Experimental Neurology 巻 80, 号 8, p. 741-753, 発行日 2021-09-10 |
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出版者 | ||||||
出版者 | Oxford University Press | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0022-3069 | |||||
PMID | ||||||
識別子タイプ | PMID | |||||
関連識別子 | 34374777 | |||||
DOI | ||||||
識別子タイプ | DOI | |||||
関連識別子 | https://doi.org/10.1093/jnen/nlab056 | |||||
関連名称 | 10.1093/jnen/nlab056 | |||||
権利 | ||||||
権利情報 | © 2021 American Association of Neuropathologists, Inc. All rights reserved. | |||||
資源タイプ | ||||||
内容記述タイプ | Other | |||||
内容記述 | Journal Article |