Jing Luan , Na Guo , Fengrui Hu , Xingchun Gou , Lixian Xu
{"title":"Aged AβPPswe/PS1ΔE9 mice as a useful animal model for studying the link between immunological senescence and diseases","authors":"Jing Luan , Na Guo , Fengrui Hu , Xingchun Gou , Lixian Xu","doi":"10.1016/j.imlet.2024.106842","DOIUrl":null,"url":null,"abstract":"<div><p>The <em>APPswe/PS1</em><strong>Δ</strong><em>E9</em> mouse is a double transgenic murine model that harbors two transgenes for Alzheimer's Disease (AD)-related mutant proteins. We previously discovered that this double transgenic animal had a premature immunosenescence phenotype. However, it is unclear how this phenotype progresses to a later stage. This study aimed to elucidate the changes in systemic characteristics aside from those associated with AD between elderly <em>APPswe/PS1</em><strong>Δ</strong><em>E9</em> mice and littermate control wild-type mice. Tumors in all organs were considerably more frequent in AD mice aged 24 months than in the control wild-type mice. In addition, the survival rate of aged AD mice was considerably lower than that of wild-type control mice. Further, we discovered that the phenotypic difference was mainly caused by severe immunological aging, as evidenced by a high proportion of exhausted T lymphocytes in AD mice compared to wild-type mice of the same age. Based on our findings, the harm produced by normal aging is not as severe as immunological senescence. Addressing immunological aging, as opposed to anti-aging alone, may be a more crucial target for a long life free of cancer.</p></div>","PeriodicalId":3,"journal":{"name":"ACS Applied Electronic Materials","volume":null,"pages":null},"PeriodicalIF":4.3000,"publicationDate":"2024-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Electronic Materials","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0165247824000166","RegionNum":3,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ENGINEERING, ELECTRICAL & ELECTRONIC","Score":null,"Total":0}
引用次数: 0
Abstract
The APPswe/PS1ΔE9 mouse is a double transgenic murine model that harbors two transgenes for Alzheimer's Disease (AD)-related mutant proteins. We previously discovered that this double transgenic animal had a premature immunosenescence phenotype. However, it is unclear how this phenotype progresses to a later stage. This study aimed to elucidate the changes in systemic characteristics aside from those associated with AD between elderly APPswe/PS1ΔE9 mice and littermate control wild-type mice. Tumors in all organs were considerably more frequent in AD mice aged 24 months than in the control wild-type mice. In addition, the survival rate of aged AD mice was considerably lower than that of wild-type control mice. Further, we discovered that the phenotypic difference was mainly caused by severe immunological aging, as evidenced by a high proportion of exhausted T lymphocytes in AD mice compared to wild-type mice of the same age. Based on our findings, the harm produced by normal aging is not as severe as immunological senescence. Addressing immunological aging, as opposed to anti-aging alone, may be a more crucial target for a long life free of cancer.
APPswe/PS1ΔE9小鼠是一种双转基因小鼠模型，它携带两种与阿尔茨海默病（AD）相关的突变蛋白的转基因。我们之前发现这种双转基因动物具有过早免疫衰老的表型。然而，目前还不清楚这种表型是如何发展到后期阶段的。本研究旨在阐明老年APPswe/PS1ΔE9小鼠与同窝对照野生型小鼠之间除与AD相关的系统特征外的变化。与对照野生型小鼠相比，24个月大的AD小鼠各器官肿瘤的发生率要高得多。此外，老年 AD 小鼠的存活率大大低于野生型对照小鼠。此外，我们发现这种表型差异主要是由严重的免疫老化引起的，与同龄的野生型小鼠相比，AD 小鼠中衰竭的 T 淋巴细胞比例较高就是证明。根据我们的研究结果，正常衰老产生的危害不如免疫衰老严重。与单纯的抗衰老相比，解决免疫衰老问题可能是实现无癌症长寿的更关键目标。
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