The 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 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.

中文翻译：

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老年 AβPPswe/PS1ΔE9 小鼠作为研究免疫衰老与疾病之间联系的有用动物模型

该小鼠是双转基因小鼠模型，含有两种与阿尔茨海默氏病（AD）相关的突变蛋白转基因。我们之前发现这种双转基因动物具有过早的免疫衰老表型。然而，尚不清楚这种表型如何进展到后期。本研究旨在阐明老年小鼠和同窝对照野生型小鼠之间除了与 AD 相关的全身特征的变化。24 个月大的 AD 小鼠所有器官中的肿瘤发生率均明显高于对照野生型小鼠。此外，老年AD小鼠的存活率明显低于野生型对照小鼠。此外，我们发现表型差异主要是由严重的免疫老化引起的，与同龄野生型小鼠相比，AD小鼠中耗竭的T淋巴细胞比例较高就证明了这一点。根据我们的研究结果，正常衰老产生的危害并不像免疫衰老那么严重。与单纯抗衰老相比，解决免疫衰老问题可能是长寿、远离癌症的更重要目标。