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dc.contributor.author | Nishioka, Hisae | en |
dc.contributor.author | Tooi, Norie | en |
dc.contributor.author | Isobe, Takehisa | en |
dc.contributor.author | Nakatsuji, Norio | en |
dc.contributor.author | Aiba, Kazuhiro | en |
dc.contributor.alternative | 饗庭, 一博 | ja |
dc.date.accessioned | 2016-10-04T00:33:24Z | - |
dc.date.available | 2016-10-04T00:33:24Z | - |
dc.date.issued | 2016-09-19 | - |
dc.identifier.issn | 2045-2322 | - |
dc.identifier.uri | http://hdl.handle.net/2433/216735 | - |
dc.description.abstract | Alzheimer's disease (AD) is the most common form of dementia. Cellular AD models derived from human pluripotent stem cells are promising tools in AD research. We recently developed human embryonic stem cell-derived AD models which overexpress mutant Presenilin1 genes, and which exhibit AD phenotypes, including synaptic dysfunction. In this study, we found that our AD models showed reduced levels of RAB3A and SV2B proteins in the pre-synapses, which is a possible cause of electrophysiological abnormalities. Through the screening of chemical compounds using our AD models, we have identified Aβ peptide inhibitors which decrease the concentration of Aβ in culture supernatant. Among these, BMS-708163 and Nilotinib were found to improve the expression levels of RAB3A and SV2B proteins and to recover the electrophysiological function in our AD models. These results suggest that the AD models we developed are promising materials for the discovery of AD drugs that target the expression of pre-synaptic proteins and synaptic function. | en |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Springer Nature | en |
dc.rights | © The Author(s) 2016. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ | en |
dc.title | BMS-708163 and Nilotinib restore synaptic dysfunction in human embryonic stem cell-derived Alzheimer's disease models | en |
dc.type | journal article | - |
dc.type.niitype | Journal Article | - |
dc.identifier.jtitle | Scientific Reports | en |
dc.identifier.volume | 6 | - |
dc.relation.doi | 10.1038/srep33427 | - |
dc.textversion | publisher | - |
dc.identifier.artnum | 33427 | - |
dc.identifier.pmid | 27641902 | - |
dcterms.accessRights | open access | - |
出現コレクション: | 学術雑誌掲載論文等 |
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