Alzheimer's disease (AD) is a multifactorial progressive neurodegenerative disease. Despite decades of research, no disease modifying therapy is available and a change of research objectives and/or development of novel research tools may be required. Much AD research has been based on experimental models using animals with a short lifespan that have been extensively genetically manipulated and do not represent the full spectrum of late-onset AD, which make up the majority of cases. The aetiology of AD is heterogeneous and involves multiple factors associated with the late-onset of the disease like disturbances in brain insulin, oxidative stress, neuroinflammation, metabolic syndrome, retinal degeneration and sleep disturbances which are all progressive abnormalities that could account for many molecular, biochemical and histopathological lesions found in brain from patients dying from AD. This review is based on the long-lived rodent Octodon degus (degu) which is a small diurnal rodent native to South America that can spontaneously develop cognitive decline with concomitant phospho-tau, β-amyloid pathology and neuroinflammation in brain. In addition, the degu can also develop several other conditions like type 2 diabetes, macular and retinal degeneration and atherosclerosis, conditions that are often associated with aging and are often comorbid with AD. Long-lived animals like the degu may provide a more realistic model to study late onset AD.

阿尔茨海默氏病（AD）是一种多因素进行性神经退行性疾病。尽管进行了数十年的研究，但尚无可用的疾病改良疗法，并且可能需要改变研究目标和/或开发新的研究工具。许多AD研究都是基于使用寿命短的动物进行的实验模型进行的，这些动物经过了广泛的基因操作，并不代表晚期AD的全部情况，这是大多数病例的原因。AD的病因学是异质的，涉及与疾病晚期相关的多种因素，例如脑胰岛素紊乱，氧化应激，神经炎症，代谢综合征，视网膜变性和睡眠障碍，这些都是进行性异常，可能导致许多分子异常，死于AD的患者在大脑中发现了生化和组织病理学损害。这篇评论是基于长寿命的啮齿动物Octodon degus（degu）是一种南美小型昼夜啮齿动物，可自发发展为认知能力下降，并伴有大脑中的磷-tau，β-淀粉样蛋白病理和神经炎症。此外，这种疾病还可能发展为其他一些疾病，如2型糖尿病，黄斑和视网膜变性和动脉粥样硬化，这些疾病通常与衰老相关，并常与AD合并。像degu这样的长寿动物可能为研究迟发性AD提供了更现实的模型。