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Mol. Neurosci."],"abstract":"<jats:p>Clinical studies have found that some Alzheimer\u2019s disease (AD) patients suffer from Cushing\u2019s syndrome (CS). CS is caused by the long-term release of excess glucocorticoids (GCs) from the adrenal gland, which in turn, impair brain function and induce dementia. Thus, we investigated the mechanism of the effect of corticosterone (CORT) on the development and progression of AD in a preclinical model. Specifically, the plasma CORT levels of 9-month-old APP\/PS1 Tg mice were abnormally increased, suggesting an association between GCs and AD. Long-term administration of CORT accelerated cognitive dysfunction by increasing the production and deposition of \u03b2-amyloid (A\u03b2). The mechanism of action of CORT treatment involved stimulation of the expression of BACE-1 and presenilin (PS) 1 in<jats:italic>in vitro<\/jats:italic>and<jats:italic>in vivo<\/jats:italic>. This observation was confirmed in mice with adrenalectomy (ADX), which had lower levels of GCs. Moreover, the glucocorticoid receptor (GR) mediated the effects of CORT on the stimulation of the expression of BACE-1 and PS1<jats:italic>via<\/jats:italic>the PKA and CREB pathways in neuroblastoma N2a cells. In addition to these mechanisms, CORT can induce a cognitive decline in APP\/PS1 Tg mice by inducing apoptosis and decreasing the differentiation of neurons.<\/jats:p>","DOI":"10.3389\/fnmol.2020.613421","type":"journal-article","created":{"date-parts":[[2021,1,15]],"date-time":"2021-01-15T05:52:30Z","timestamp":1610689950000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":12,"title":["The Molecular Mechanism of Chronic High-Dose Corticosterone-Induced Aggravation of Cognitive Impairment in APP\/PS1 Transgenic Mice"],"prefix":"10.3389","volume":"13","author":[{"given":"Shen-Qing","family":"Zhang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Long-Long","family":"Cao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yun-Yue","family":"Liang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pu","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2021,1,15]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"9","DOI":"10.1016\/j.bbi.2019.01.004","article-title":"CREB signals as PBMC-based biomarkers of cognitive dysfunction: a novel perspective of the brain-immune axis","volume":"78","author":"Bartolotti","year":"2019","journal-title":"Brain Behav. 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