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dc.contributor.author한평림-
dc.date.accessioned2020-07-10T16:30:11Z-
dc.date.available2020-07-10T16:30:11Z-
dc.date.issued2020-
dc.identifier.issn2399-3642-
dc.identifier.otherOAK-27080-
dc.identifier.urihttp://dspace.ewha.ac.kr/handle/2015.oak/254106-
dc.description.abstractBrain aging proceeds with cellular and molecular changes in the limbic system. Aging-dependent changes might affect emotion and stress coping, yet the underlying mechanisms remain unclear. Here, we show aged (18-month-old) mice exhibit upregulation of NADPH oxidase and oxidative stress in the hippocampus, which mirrors the changes in young (2-month-old) mice subjected to chronic stress. Aged mice that lack p47phox, a key subunit of NADPH oxidase, do not show increased oxidative stress. Aged mice exhibit depression-like behavior following weak stress that does not produce depressive behavior in young mice. Aged mice have reduced expression of the epigenetic factor SUV39H1 and its upstream regulator p-AMPK, and increased expression of Ppp2ca in the hippocampus—changes that occur in young mice exposed to chronic stress. SUV39H1 mediates stress- and aging-induced sustained upregulation of p47phox and oxidative stress. These results suggest that aging increases susceptibility to stress by upregulating NADPH oxidase in the hippocampus. © 2020, The Author(s).-
dc.languageEnglish-
dc.publisherNature Research-
dc.titleAging increases vulnerability to stress-induced depression via upregulation of NADPH oxidase in mice-
dc.typeArticle-
dc.relation.issue1-
dc.relation.volume3-
dc.relation.indexSCOPUS-
dc.relation.journaltitleCommunications Biology-
dc.identifier.doi10.1038/s42003-020-1010-5-
dc.identifier.wosidWOS:000540512500002-
dc.identifier.scopusid2-s2.0-85085984618-
dc.author.googleLee J.-E.-
dc.author.googleKwon H.-J.-
dc.author.googleChoi J.-
dc.author.googleSeo J.-S.-
dc.author.googleHan P.-L.-
dc.contributor.scopusid한평림(7201947605)-
dc.date.modifydate20200813132219-
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일반대학원 > 뇌·인지과학과 > Journal papers
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