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j.bbrc.2015.12.025.pdf | 1.05 MB | Adobe PDF | 見る/開く |
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dc.contributor.author | Honda, Makoto | en |
dc.contributor.author | Minami, Itsunari | en |
dc.contributor.author | Tooi, Norie | en |
dc.contributor.author | Morone, Nobuhiro | en |
dc.contributor.author | Nishioka, Hisae | en |
dc.contributor.author | Uemura, Kengo | en |
dc.contributor.author | Kinoshita, Ayae | en |
dc.contributor.author | Heuser, John E. | en |
dc.contributor.author | Nakatsuji, Norio | en |
dc.contributor.author | Aiba, Kazuhiro | en |
dc.date.accessioned | 2017-03-01T02:39:20Z | - |
dc.date.available | 2017-03-01T02:39:20Z | - |
dc.date.issued | 2016-01-15 | - |
dc.identifier.issn | 1090-2104 | - |
dc.identifier.uri | http://hdl.handle.net/2433/218506 | - |
dc.description.abstract | Cellular disease models are useful tools for Alzheimer's disease (AD) research. Pluripotent stem cells, including human embryonic stem cells (hESCs) and induced pluripotent stem cells (iPSCs), are promising materials for creating cellular models of such diseases. In the present study, we established cellular models of AD in hESCs that overexpressed the mutant Presenilin 1 (PS1) gene with the use of a site-specific gene integration system. The overexpression of PS1 did not affect the undifferentiated status or the neural differentiation ability of the hESCs. We found increases in the ratios of amyloid-β 42 (Aβ42)/Aβ40 and Aβ43/Aβ40. Furthermore, synaptic dysfunction was observed in a cellular model of AD that overexpressed mutant PS1. These results suggest that the AD phenotypes, in particular, the electrophysiological abnormality of the synapses in our AD models might be useful for AD research and drug discovery. | en |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Academic Press Inc. | en |
dc.rights | © 2015 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). | en |
dc.subject | Alzheimer's disease | en |
dc.subject | Cellular disease model | en |
dc.subject | Human embryonic stem cell | en |
dc.subject | Presenilin 1 | en |
dc.subject | Synaptic dysfunction | en |
dc.title | The modeling of Alzheimer's disease by the overexpression of mutant Presenilin 1 in human embryonic stem cells | en |
dc.type | journal article | - |
dc.type.niitype | Journal Article | - |
dc.identifier.jtitle | Biochemical and Biophysical Research Communications | en |
dc.identifier.volume | 469 | - |
dc.identifier.spage | 587 | - |
dc.identifier.epage | 592 | - |
dc.relation.doi | 10.1016/j.bbrc.2015.12.025 | - |
dc.textversion | publisher | - |
dc.address | Institute for Integrated Cell-Material Sciences (WPI-iCeMS), Kyoto University | en |
dc.address | Department of Neurology, Kyoto University Graduate School of Medicine | en |
dc.address | School of Human Health Sciences, Kyoto University Graduate School of Medicine | en |
dc.address | Institute for Frontier Medical Sciences, Kyoto University | en |
dc.identifier.pmid | 26687948 | - |
dcterms.accessRights | open access | - |
dc.identifier.pissn | 0006-291X | - |
出現コレクション: | 学術雑誌掲載論文等 |
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